Relation Results

Identifier	Residue	Sequence
SIGNOR-275891	Lys3016	VLMRLQEkLKGVEEG
pmid	sentence
30944854	Here, we report that sirtuin 7 (SIRT7)-mediated deacetylation is essential for dephosphorylation and deactivation of ATM. We show that SIRT7, a class III histone deacetylase, interacts with and deacetylates ATM in vitro and in vivo. \|Upon DNA damage, ATM is activated via a series of highly organized machineries, including acetylation by the histone acetyltransferase TIP60 at lysine 3016

Publications:

1

Identifier	Residue	Sequence
SIGNOR-275890	Lys3016	VLMRLQEkLKGVEEG
pmid	sentence
30944854	Here, we report that sirtuin 7 (SIRT7)-mediated deacetylation is essential for dephosphorylation and deactivation of ATM. We show that SIRT7, a class III histone deacetylase, interacts with and deacetylates ATM in vitro and in vivo. \|Upon DNA damage, ATM is activated via a series of highly organized machineries, including acetylation by the histone acetyltransferase TIP60 at lysine 3016

Publications:

1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273508	Ser1003	TKSTIKPsQMSVARI	Homo sapiens	HEK-293 Cell
pmid	sentence
33097710	Here, we identify that USP52 directly interacts with and deubiquitinates CtIP, thereby promoting DNA end resection and HR. Mechanistically, USP52 removes the ubiquitination of CtIP to facilitate the phosphorylation and activation of CtIP at Thr-847. In addition, USP52 is phosphorylated by ATM at Ser-1003 after DNA damage, which enhances the catalytic activity of USP52.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-179435	Ser101	DLTATQLsQGANGWQ	Homo sapiens
pmid	sentence
18619531	Thus, phosphorylation of ser-101 on sp1 is a general response to dna damage, dependent on both atm and atr.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-273433	Ser1037	IGNSNHGsQSPRNVE
pmid	sentence
29939287	To investigate to what extent EVI1 function might be regulated by post-translational modifications we carried out mass spectrometry- and antibody-based analyses and uncovered an ATM-mediated double phosphorylation of EVI1 at the carboxy-terminal S858/S860 SQS motif.

Identifier	Residue	Sequence
SIGNOR-273434	Ser1039	NSNHGSQsPRNVEER
pmid	sentence
29939287	To investigate to what extent EVI1 function might be regulated by post-translational modifications we carried out mass spectrometry- and antibody-based analyses and uncovered an ATM-mediated double phosphorylation of EVI1 at the carboxy-terminal S858/S860 SQS motif.

Publications:

2

Identifier	Residue	Sequence	Organism
SIGNOR-165567	Ser106	GPGQVMAsQAQQSSP	Homo sapiens
pmid	sentence
20471956	Atm mediates phosphorylation of p300 in response to dna damageexpression of nonphosphorylatable serine to alanine form of p300 (s106a) destabilized both p300 and nbs1 proteins, after dna damage

Publications:

1

Organism:

Homo Sapiens

Pathways:

p53 in cancer

Identifier	Residue	Sequence	Organism
SIGNOR-124047	Ser107	SVDSVTDsQKRREIL	Homo sapiens
pmid	sentence
15073328	Atm phosphorylated creb in vitro and in vivo in response to ionizing radiation (ir) and h(2)o(2) on a stress-inducible domain. Ir-induced phosphorylation of creb correlated with a decrease in creb transactivation potential and reduced interaction between creb and its transcriptional coactivator, creb-binding protein (cbp). A creb mutant containing ala substitutions at atm phosphorylation sites displayed enhanced transactivation potential,

Identifier	Residue	Sequence	Organism
SIGNOR-124051	Thr100	LKRLFSGtQISTIAE	Homo sapiens
pmid	sentence
15073328	Individual ala substitutions at thr-100, ser-111, or ser-121 inhibited atm-catalyzed phosphate incorporationatm phosphorylated creb in vitro and in vivo in response to ionizing radiation (ir) and h(2)o(2) on a stress-inducible domain. Ir-induced phosphorylation of creb correlated with a decrease in creb transactivation potential and reduced interaction between creb and its transcriptional coactivator, creb-binding protein (cbp)

Publications:

2

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism
SIGNOR-178479	Ser1083	ESERGSGsQSSVPSV	Homo sapiens
pmid	sentence
18442975	Ser-1083 phosphorylation is ir-inducible, depends on atm and nijmegen breakage syndrome 1 (nbs1), and is required for intra-s phase checkpoint.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-85619	Ser112	KRAGGEEsQFEMDI	Homo sapiens
pmid	sentence
11146653	Here we report that atm... phosphorylates 4e-bp1 at ser 111cells lacking atm kinase activity exhibit a significant decrease in the insulin-induced dissociation of 4e-bp1 from eif-4e.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-277510	Ser1135	HDDSSSDsGTPSGPD	Homo sapiens
pmid	sentence
32015321	Specifically, DNA damage signal, triggered by teniposide (VM-26) treatment, activates ATM, cooperating with CK1 to phosphorylate TOP2β on Ser1134 and Ser1130, respectively, in a canonical degron motif to facilitate β-TrCP binding and subsequent degradation.ATM binds with and phosphorylates TOP2β at Ser1134 to promote its degradation by VM-26.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276315	Ser114	ALLRCHEsQGELSSA	Homo sapiens	HEK-293 Cell
pmid	sentence
21362549	ATM-Mediated Phosphorylation of RNF20 and RNF40 in Response to DNA Damage and Its Requirement for Damage-Induced H2B Monoubiquitylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-176008	Ser114	EETRTPEsQPDTPPG	Homo sapiens
pmid	sentence
21824916	We demonstrate that pnkp is phosphorylated by the dna-dependent protein kinase (dna-pk) and ataxia-telangiectasia mutated (atm) in vitro. The major phosphorylation site for both kinases was serine 114, with serine 126 being a minor site. Purified pnkp protein with mutation of serines 114 and 126 had decreased dna kinase and dna phosphatase activities and reduced affinity for dna in vitro.

Identifier	Residue	Sequence	Organism
SIGNOR-176012	Ser126	PPGTPLVsQDEKRDA	Homo sapiens
pmid	sentence
21824916	We demonstrate that pnkp is phosphorylated by the dna-dependent protein kinase (dna-pk) and ataxia-telangiectasia mutated (atm) in vitro. The major phosphorylation site for both kinases was serine 114, with serine 126 being a minor site. Purified pnkp protein with mutation of serines 114 and 126 had decreased dna kinase and dna phosphatase activities and reduced affinity for dna in vitro.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250577	Ser1141	PEKAYSSsQPVISAQ	in vitro
pmid	sentence
10608806	We determined a general phosphorylation consensus sequence for ATM and identified putative in vitro targets by using glutathione S-transferase peptides as substrates. Putative ATM in vitro targets include p95/nibrin, Mre11, Brca1, Rad17, PTS, WRN, and ATM (S440) itself.

Identifier	Residue	Sequence	Organism
SIGNOR-250578	Ser1292	MTIGMHLsQAVKAGC	in vitro
pmid	sentence
10608806	We determined a general phosphorylation consensus sequence for ATM and identified putative in vitro targets by using glutathione S-transferase peptides as substrates. Putative ATM in vitro targets include p95/nibrin, Mre11, Brca1, Rad17, PTS, WRN, and ATM (S440) itself.

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-125073	Ser1197	HIQTPMLsQEQAQPP	Homo sapiens
pmid	sentence
15173573	Tonebp/orebp contains atm consensus phosphorylation sites at ser-1197, ser-1247, and ser-1367. In conclusion, signaling via atm is necessary for full activation of tonebp/orebp

Identifier	Residue	Sequence	Organism
SIGNOR-125077	Ser1247	AMQSNSPsQEQQQQQ	Homo sapiens
pmid	sentence
15173573	Tonebp/orebp contains atm consensus phosphorylation sites at ser-1197, ser-1247, and ser-1367. In conclusion, signaling via atm is necessary for full activation of tonebp/orebp

Identifier	Residue	Sequence	Organism
SIGNOR-125081	Ser1367	LVQGSPSsQEQQVTL	Homo sapiens
pmid	sentence
15173573	Tonebp/orebp contains atm consensus phosphorylation sites at ser-1197, ser-1247, and ser-1367. In conclusion, signaling via atm is necessary for full activation of tonebp/orebp

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-197611	Ser1219	DDTESLHsQGEEEFD	Homo sapiens
pmid	sentence
22621922	Here we report phosphorylation of 53bp1 at several novel residues, using mass spectrometry and phospho-specific antibodies, and show that ionising radiation-stimulated phosphorylation of these residues requires atm.

Identifier	Residue	Sequence	Organism
SIGNOR-197615	Ser831	EPVEQDSsQPSLPLV	Homo sapiens
pmid	sentence
22621922	Here we report phosphorylation of 53bp1 at several novel residues, using mass spectrometry and phospho-specific antibodies, and show that ionising radiation-stimulated phosphorylation of these residues requires atm.

Identifier	Residue	Sequence	Organism
SIGNOR-197619	Thr302	PEPEVLStQEDLFDQ	Homo sapiens
pmid	sentence
22621922	Here we report phosphorylation of 53bp1 at several novel residues, using mass spectrometry and phospho-specific antibodies, and show that ionising radiation-stimulated phosphorylation of these residues requires atm.

Identifier	Residue	Organism
SIGNOR-197622		Homo sapiens
pmid	sentence
22621922	The kinase vrk1 is activated by dna double strand breaks induced by ionizing radiation (ir) and specifically phosphorylates 53bp1 in serum-starved cells.

Publications:

4

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72048	Ser1330	QMRHQSEsQGVGLSD	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-91482	Ser1387	EDCSGLSsQSDILTT	Homo sapiens	Breast Cancer Cell
pmid	sentence
12183412	Phosphorylation of serine 1387 in brca1 is specifically required for the atm-mediated s-phase checkpoint after ionizing irradiation.We recently reported that brca1 function is required for appropriate cell cycle arrests after ionizing irradiation in both the s-phase and the g2 phase of the cell cycle. We also found that mutation of serine 1423 in brca1, a target of atm phosphorylation, abrogates the g2-m checkpoint but not the ionizing irradiation-induced s-phase checkpoint. Here we demonstrate that mutation of serine 1387 in brca1, another target of atm phosphorylation, conversely abrogates the radiation-induced s-phase arrest but does not affect the g2-m checkpoint.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72052	Ser1423	AVLEQHGsQPSNSYP	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	Phosphorylation of serine 1387 in brca1 is specifically required for the atm-mediated s-phase checkpoint after ionizing irradiation.We recently reported that brca1 function is required for appropriate cell cycle arrests after ionizing irradiation in both the s-phase and the g2 phase of the cell cycle. We also found that mutation of serine 1423 in brca1, a target of atm phosphorylation, abrogates the g2-m checkpoint but not the ionizing irradiation-induced s-phase checkpoint. Here we demonstrate that mutation of serine 1387 in brca1, another target of atm phosphorylation, conversely abrogates the radiation-induced s-phase arrest but does not affect the g2-m checkpoint.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72056	Ser1457	SEKAVLTsQKSSEYP	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72060	Ser1466	KSSEYPIsQNPEGLS	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-187591	Ser1497	EPGVERSsPSKCPSL	Homo sapiens	Lung Cancer Cell
pmid	sentence
19683496	However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72064	Ser1497	EPGVERSsPSKCPSL	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72068	Ser1524	LQNRNYPsQEELIKV	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks. Phosphorylation of brca1 on ser1423 and ser1524 by atm

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72072	Ser1542	EEQQLEEsGPHDLTE	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks. Phosphorylation of brca1 on ser1423 and ser1524 by atm

Identifier	Residue	Organism
SIGNOR-87845		Homo sapiens
pmid	sentence
12024016	Results from this study indicate that the checkpoint protein kinase atm (mutated in ataxia telangiectasia) was required for phosphorylation of brca1 in response to ionizing radiation. Brca1 is phosphorylated at tyrosine residues in an atm-dependent, radiation-dependent manner.

Identifier	Residue	Organism	Cell Line
SIGNOR-72075		Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	Results from this study indicate that the checkpoint protein kinase atm (mutated in ataxia telangiectasia) was required for phosphorylation of brca1 in response to ionizing radiation. Brca1 is phosphorylated at tyrosine residues in an atm-dependent, radiation-dependent manner.

Publications:

11

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer, Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism
SIGNOR-161934	Ser135	EWETPDLsQAEIEQK	Homo sapiens
pmid	sentence
19962312	We show that, upon dna damage, rassf1a is phosphorylated by atm on ser131 and is involved in the activation of both mst2 and lats1, leading to the stabilization of p73.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277582	Ser135	PCNAGTFsQPEKVYT	Homo sapiens	HeLa Cell
pmid	sentence
35085551	Taken together, we highlight the functional significance of the crosstalk between the kinetochore-oriented signal and double-strand break repair pathways via ATM phosphorylation of Bub3 on Ser135.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-262636	Ser135	VNNESGEsQRGTDFS	in vitro
pmid	sentence
18571408	Aven is also a substrate of the ATM kinase. Mutation of ATM-mediated phosphorylation sites on Aven reduced its ability to activate ATM, suggesting that Aven activation of ATM after DNA damage is enhanced by ATM-mediated Aven phosphorylation. We found that mutating S135 and S308 sites to Alanine largely dampened Aven’s phosphorylation by ATM (though some phosphorylation remained, due to either a contaminating kinase or an unidentified ATM phosphorylation site).

Identifier	Residue	Sequence	Organism
SIGNOR-262637	Ser308	NILPDQTsQDLKSKE	in vitro
pmid	sentence
18571408	Aven is also a substrate of the ATM kinase. Mutation of ATM-mediated phosphorylation sites on Aven reduced its ability to activate ATM, suggesting that Aven activation of ATM after DNA damage is enhanced by ATM-mediated Aven phosphorylation. We found that mutating S135 and S308 sites to Alanine largely dampened Aven’s phosphorylation by ATM (though some phosphorylation remained, due to either a contaminating kinase or an unidentified ATM phosphorylation site).

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-160206	Ser140	GKKATQAsQEY	Homo sapiens
pmid	sentence
18158901	H2ax interacts with numerous proteins required for dna damage signaling and repair when phosphorylated on ser-140. Phosphorylation of ser-140 (h2ax139ph) in response to ionizing radiation is mediated by both atm and prkdc. Our data showed that h2ax is phosphorylated by uva-activated jnk.

Identifier	Residue	Sequence	Organism
SIGNOR-174442	Ser140	GKKATQAsQEY	Homo sapiens
pmid	sentence
21690091	Upon dna damage, h2ax is phosphorylated by ataxia telangiectasia mutated (atm) and atm-related kinases at serine 139, known as ?_?_?_-H2ax, which serves as a docking site to recruit the mediator of dna damage checkpoint protein 1 (mdc1) to sites of dna damage, named dna damage foci

Publications:

2

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism
SIGNOR-90109	Ser1401	LQGEEIKsQNSQEST	Homo sapiens
pmid	sentence
12086603	These results suggest that s222 and either s1401, s1404, or s1408 are sites of atm-dependent phosphorylation in vitro.Phosphorylation Of fancd2 is required for activation of an s phase checkpoint

Identifier	Residue	Sequence	Organism
SIGNOR-90113	Ser1404	EEIKSQNsQESTADE	Homo sapiens
pmid	sentence
12086603	These results suggest that s222 and either s1401, s1404, or s1408 are sites of atm-dependent phosphorylation in vitro.Phosphorylation Of fancd2 is required for activation of an s phase checkpoint

Identifier	Residue	Sequence	Organism
SIGNOR-90117	Ser1407	KSQNSQEsTADESED	Homo sapiens
pmid	sentence
12086603	These results suggest that s222 and either s1401, s1404, or s1408 are sites of atm-dependent phosphorylation in vitro.Phosphorylation Of fancd2 is required for activation of an s phase checkpoint

Identifier	Residue	Sequence	Organism
SIGNOR-90121	Ser222	LPEILGDsQHADVGK	Homo sapiens
pmid	sentence
12086603	Atm phosphorylates fancd2 on serine 222 in vitro. This site is also phosphorylated in vivo in an atm-dependent manner following ir. Phosphorylation of fancd2 is required for activation of an s phase checkpoint. The atm-dependent phosphorylation of fancd2 on s222 and the fa pathway-dependent monoubiquitination of fancd2 on k561 are independent posttranslational modifications regulating discrete cellular signaling pathways.

Publications:

4

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-177280	Ser1403	CHKTKLKsILEILSK	Homo sapiens
pmid	sentence
22099307	Aurora-b mediated atm serine 1403 phosphorylation is required for mitotic atm activation and the spindle checkpoint

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262792	Ser141	DYNETDWsQEFISEV	Homo sapiens	HEK-293 Cell
pmid	sentence
26344566	Specificity for autophagy of peroxisomes (pexophagy) is provided by ATM phosphorylation of PEX5 at Ser 141, which promotes PEX5 monoubiquitylation at Lys 209, and recognition of ubiquitylated PEX5 by the autophagy adaptor protein p62, directing the autophagosome to peroxisomes to induce pexophagy.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-182949	Ser1449	AAPDADLsQEPHLF	Homo sapiens
pmid	sentence
19109555	The s1449a mutant failed to completely correct a variety of fa-associated phenotypes. The dna damage response is coordinated by phosphorylation events initiated by apical kinases atm (ataxia telangectasia mutated) and atr (atm and rad3-related), and atr is essential for proper fa pathway function. Serine 1449 is in a consensus atm/atr site

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-126753	Ser15	PSVEPPLsQETFSDL	Homo sapiens	HaCaT Cell
pmid	sentence
15254178	Deltanp63 transcriptionally regulates atm to control p53 serine-15 phosphorylation. We next aimed to identify novel factors that control damage-induced p53 phosphorylation in a keratinocyte model system, and discovered that the epithelial stem cell marker _Np63_ is a novel ATM regulator that controls p53 Serine-15 phosphorylation through transcription of the ATM kinase.

Identifier	Residue	Sequence	Organism
SIGNOR-115340	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
11875057	In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization.

Identifier	Residue	Sequence	Organism
SIGNOR-158632	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
17967874	In this study, we show that the increased interaction between B56gamma and p53 after DNA damage requires ATM-dependent phosphorylation of p53 at Ser15.

Identifier	Residue	Sequence	Organism
SIGNOR-167152	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
20663147	Deltanp63 transcriptionally regulates atm to control p53 serine-15 phosphorylation.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-167156	Ser20	PLSQETFsDLWKLLP	Homo sapiens	HaCaT Cell
pmid	sentence
20663147	DeltaNp63alpha depletion by RNAi reduces steady-state ATM mRNA and protein levels, and attenuates p53 Serine-15 phosphorylation. Conversely, ectopic expression of DeltaNp63alpha in p63-null tumour cells stimulates ATM transcription and p53 Serine-15 phosphorylation

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-158636	Ser20	PLSQETFsDLWKLLP	Homo sapiens	NCI-H1299 Cell
pmid	sentence
17967874	The increased interaction between B56gamma and p53 after DNA damage requires ATM-dependent phosphorylation of p53 at Ser15.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-126757	Ser20	PLSQETFsDLWKLLP	Homo sapiens	U2-OS Cell
pmid	sentence
15254178	Although the stabilization of p53 was apparently concordant with its phosphorylation on N-terminal serine residues in HFFF-2 cells, it did not require the phosphorylation of Ser15 or Ser20 by ATM, a cellular kinase known to phosphorylate and promote the stabilization of p53 in response to DNA damage.

Identifier	Residue	Sequence	Organism
SIGNOR-115344	Ser46	AMDDLMLsPDDIEQW	Homo sapiens
pmid	sentence
11875057	In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization.

Identifier	Residue	Sequence	Organism
SIGNOR-115348	Ser9	EEPQSDPsVEPPLSQ	Homo sapiens
pmid	sentence
11875057	In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization.

Identifier	Residue	Organism
SIGNOR-151138		Homo sapiens
pmid	sentence
17157788	Atm/atr are generally sensors of dna damage, but, together with the checkpoint kinases chk1 and chk2, they also function as response effectors by phosphorylation of key substrates, such as p53, brca1, and nbs1. In particular, p53 phosphorylation leads to protein accumulation and activation, which in turn promotes cell-cycle arrest or apoptosis.

Publications:

10

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-72079	Ser1524	LQNRNYPsQEELIKV	Homo sapiens	Breast Cancer Cell
pmid	sentence
10550055	The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. Results from this study indicate that the checkpoint protein kinase atm (mutated in ataxia telangiectasia) was required for phosphorylation of brca1 in response to ionizing radiation. Atm resides in a complex with brca1 and phosphorylated brca1 in vivo and in vitro in a region that contains clusters of serine-glutamine residues. Phosphorylation of this domain appears to be functionally important because a mutated brca1 protein lacking two phosphorylation sites failed to rescue the radiation hypersensitivity of a brca1-deficient cell line.Atm-dependent phosphorylation of ser1423 or ser1524 also occurred in vivo,

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer, Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277549	Ser158	EFVEHLIsQMCHYQH	Homo sapiens	MCF-7 Cell
pmid	sentence
33676897	ATM phosphorylates and stabilizes β-TrCP1 upon DNA damage.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-276488	Ser162	TCSENGVsLCLPRLE	Homo sapiens
pmid	sentence
23435430	Here we uncover ATM as a novel positive modulator of ITCH E3-ubiquitin ligase activity. A single residue on ITCH protein, S161, which is part of an ATM SQ consensus motif, is required for ATM-dependent activation of ITCH.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276314	Ser172	SSSEEMEsQLQERVE	Homo sapiens	HEK-293 Cell
pmid	sentence
21362549	ATM-Mediated Phosphorylation of RNF20 and RNF40 in Response to DNA Damage and Its Requirement for Damage-Induced H2B Monoubiquitylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250579	Ser173	VKKNPHHsQWGDMKL	in vitro
pmid	sentence
16540648	Kinase phosphorylation assays were done with synthesized short peptides (20-mer) with the sequences at Ser173 and Ser196 of XPA, respectively. Both peptides seemed to be good substrates for DNA-PK, ATR ( Fig. 2D), and ATM (data not shown).

Identifier	Residue	Sequence	Organism
SIGNOR-250580	Ser196	RSLEVWGsQEALEEA	in vitro
pmid	sentence
16540648	Kinase phosphorylation assays were done with synthesized short peptides (20-mer) with the sequences at Ser173 and Ser196 of XPA, respectively. Both peptides seemed to be good substrates for DNA-PK, ATR ( Fig. 2D), and ATM (data not shown).

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-255591	Ser183	GTGEEPGsQGLNGEA	in vitro
pmid	sentence
26324325	ATM indeed mediated PPM1G phosphorylation at S183, and mutation of this residue (S183A) abrogated detection with the phospho-specific antibody

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264415	Ser189	EGDDAEDsQGESEED	Homo sapiens	HCT-116 Cell
pmid	sentence
17157788	The checkpoint kinases ATM/ATR and Chk2 interact with Che-1 and promote its phosphorylation and accumulation in response to DNA damage. These Che-1 modifications induce a specific recruitment of Che-1 on the TP53 and p21 promoters. \|DNA damage stabilizes Che-1 protein\|In addition, substitution of Che-1 Ser187 with an alanine (Che-1S187A) prevented Che-1 phosphorylation by ATM (Figure 2F), supporting this residue as an ATM-target site.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-170465	Ser1893	PANLDSEsEHFFRCC	Homo sapiens
pmid	sentence
21149446	In human cells, the activation process involves autophosphorylation on three sites (ser367, ser1893, and ser1981) and acetylation on lys3016. We now describe the identification of a new atm phosphorylation site, thr(p)1885 and an additional autophosphorylation site, ser(p)2996, that is highly dna damage-inducible.

Identifier	Residue	Sequence	Organism
SIGNOR-170469	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
21149446	In human cells, the activation process involves autophosphorylation on three sites (ser367, ser1893, and ser1981) and acetylation on lys3016. We now describe the identification of a new atm phosphorylation site, thr(p)1885 and an additional autophosphorylation site, ser(p)2996, that is highly dna damage-inducible.

Identifier	Residue	Sequence	Organism
SIGNOR-170473	Ser2996	QECKRNLsDIDQSFN	Homo sapiens
pmid	sentence
21149446	In human cells, the activation process involves autophosphorylation on three sites (ser367, ser1893, and ser1981) and acetylation on lys3016. We now describe the identification of a new atm phosphorylation site, thr(p)1885 and an additional autophosphorylation site, ser(p)2996, that is highly dna damage-inducible.

Identifier	Residue	Sequence	Organism
SIGNOR-170477	Ser367	DTRSLEIsQSYTTTQ	Homo sapiens
pmid	sentence
21149446	In human cells, the activation process involves autophosphorylation on three sites (ser367, ser1893, and ser1981) and acetylation on lys3016. We now describe the identification of a new atm phosphorylation site, thr(p)1885 and an additional autophosphorylation site, ser(p)2996, that is highly dna damage-inducible.

Publications:

4

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81391	Ser19	SHGSSACsQPHGSVT	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81395	Ser28	PHGSVTQsQGSSSQS	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to irser28 was also found to be phosphorylated in an atm-dependent manner

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81399	Ser33	TQSQGSSsQSQGISS	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81403	Ser35	SQGSSSQsQGISSSS	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81407	Ser50	TSTMPNSsQSSHSSS	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to iratm- and rad3-related also phosphorylates thr68 in addition to thr26 and ser50, which are not phosphorylated to a significant extent by atm in vitro.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-87850	Thr26	SQPHGSVtQSQGSSS	Homo sapiens	HEK-293 Cell
pmid	sentence
12024051	We show here that autophosphorylation of chk2 produced in a cell-free system requires trans phosphorylation by a wortmannin-sensitive kinase, probably atm or atr

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-81438	Thr68	SSLETVStQELYSIP	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Here we show that in vitro, atm phosphorylates the ser-gln/thr-gln (sq/tq) cluster domain (scd) on chk2, which contains seven sq/tq motifs, and thr68 is the major in vitro phosphorylation site by atm. Atm predominantly phosphorylates chk2 at thr68, promoting homodimerization and activation via intramolecular trans-autophosphorylation at thr383/387.

Identifier	Residue	Sequence	Organism
SIGNOR-276053	Thr68	SSLETVStQELYSIP	in vitro
pmid	sentence
16481012	Plk3 phosphorylates Chk2 at two residues, serine 62 (S62) and serine 73 (S73) in vitro, and this phosphorylation facilitates subsequent phosphorylation of Chk2 on T68 by ATM in response to DNA damage. When the Chk2 mutant construct GFP-Chk2 S73A (serine 73 mutated to alanine) is transfected into cells, it no longer associates with a large complex in vivo, and manifests a significant reduction in kinase activity.

Publications:

8

Organism:

Homo Sapiens, In Vitro

Pathways:

DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence	Organism
SIGNOR-177945	Ser19	GTSKCPPsQRVPALT	Homo sapiens
pmid	sentence
18536714	Disruption of the hipk2-siah-1 complex is mediated by the atm/atr pathway and involves atm/atr-dependent phosphorylation of siah-1 at ser 19.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-248601	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
15510216	Ionizing radiation induces autophosphorylation of the ataxia-telangiectasia mutated (ATM) protein kinase on serine 1981; however, the precise mechanisms that regulate ATM activation are not fully understood. Here, we show that the protein phosphatase inhibitor okadaic acid (OA) induces autophosphorylation of ATM on serine 1981 in unirradiated cells at concentrations that inhibit protein phosphatase 2A-like activity in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-150870	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
17124492	Atr-dependent phosphorylation and activation of atm in response to uv treatment or replication fork stalling. Here, we show that atm phosphorylation at ser1981, a characterised autophosphorylation site, is atr-dependent and atm-independent following replication fork stalling or uv treatment

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence	Organism
SIGNOR-276954	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
18265945	More recently, Shreeram et al. have also shown that Wip1 dephosphorylates human ATM at Ser367 as well as Ser1981.\|Thus, overexpression of Wip1 in an oncogenic context could contribute to tumor promotion by inhibiting both p53 and ATM functions.

Identifier	Residue	Sequence	Organism
SIGNOR-248325	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
16949371	Here, we report that deficiency of Wip1 resulted in activation of the ataxia-telangiectasia mutated (ATM) kinase. In turn, overexpression of Wip1 was sufficient to reduce activation of the ATM-dependent signaling cascade after DNA damage. Wip1 dephosphorylated ATM Ser1981, a site critical for ATM monomerization and activation

Identifier	Residue	Sequence	Organism
SIGNOR-276955	Ser367	DTRSLEIsQSYTTTQ	Homo sapiens
pmid	sentence
18265945	More recently, Shreeram et al. have also shown that Wip1 dephosphorylates human ATM at Ser367 as well as Ser1981.\|Thus, overexpression of Wip1 in an oncogenic context could contribute to tumor promotion by inhibiting both p53 and ATM functions.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-248644	Ser1981	SLAFEEGsQSTTISS	Homo sapiens
pmid	sentence
15510216	Ionizing radiation induces autophosphorylation of the ataxia-telangiectasia mutated (ATM) protein kinase on serine 1981; however, the precise mechanisms that regulate ATM activation are not fully understood. Here, we show that the protein phosphatase inhibitor okadaic acid (OA) induces autophosphorylation of ATM on serine 1981 in unirradiated cells at concentrations that inhibit protein phosphatase 2A-like activity in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-155634	Ser202	GEKPFQCsQCDMRFI	Homo sapiens
pmid	sentence
17560543	Here we found that zbp-89 is phosphorylated by atm kinase in vitro and in vivo. Disruption of the atm phosphorylation motif (202)sq within the zinc finger domain of zbp-89 attenuated its ability to enhance p21(waf1) activation by butyrate. Moreover, disruption of the atm phosphorylation site abrogated the ability of zbp-89 to potentiate butyrate induction of endogenous p21(waf1) expression.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-262645	Ser203	TGQNPKIsQQALSAY	Homo sapiens
pmid	sentence
15448695	Here we report a new pathway in which ATM kinase signals the DNA damage response by targeting the transcriptional cofactor Strap. ATM phosphorylates Strap at a serine residue, stabilizing nuclear Strap and facilitating formation of a stress-responsive co-activator complex.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-108419	Ser219	SKLLMIIsQKDTFHS	Homo sapiens	HeLa Cell
pmid	sentence
11375976	Telomeric protein pin2/trf1 as an important atm target in response to double strand dna breaks. activated atm directly phosphorylated pin2/trf1 preferentially on the conserved ser(219)-gln site in vitro and in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273506	Ser233	ARLHTKPsQAPAVEV	Homo sapiens	HEK-293 Cell
pmid	sentence
27829214	PICT-1 S233 and T289 were identified as the key phosphorylation sites in this pathway, as mutating both to alanine abolished UVB-induced increase of PICT-1 phosporylation. Inhibition of PIKKs or ATM (with wortmannin and KU55933, respectively) prevented the agglomeration and degradation of PICT-1, suggesting that ATM is a key regulator of PICT-1.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273507	Thr289	PATEQAAtQESTFQE	Homo sapiens	HEK-293 Cell
pmid	sentence
27829214	PICT-1 S233 and T289 were identified as the key phosphorylation sites in this pathway, as mutating both to alanine abolished UVB-induced increase of PICT-1 phosporylation. Inhibition of PIKKs or ATM (with wortmannin and KU55933, respectively) prevented the agglomeration and degradation of PICT-1, suggesting that ATM is a key regulator of PICT-1.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-197533	Ser239	DPMTQDGsQPMDTNM	Homo sapiens
pmid	sentence
22588298	On genotoxic stress, atm phosphorylates bmps-activated smad1 in the nucleus on s239, which disrupts smad1 interaction with protein phosphatase ppm1a, leading to enhanced activation and upregulation of smad1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-205087	Ser249	IQRGVSPsQAQGLGS	Homo sapiens
pmid	sentence
24821553	Serine 249 phosphorylation by atm protein kinase regulates hepatocyte nuclear factor-1_ transactivation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-100641	Ser25	PCLIIEDsQPESQVL	Homo sapiens
pmid	sentence
12697768	To examine whether the respective sq sites become phosphorylated in vivo, we raised polyclonal antibodies against phosphorylated ser-6 (anti-s6p), phosphorylated ser-25 and ser-29 (anti-s25p/29p), and phosphorylated ser-784 (anti-s784p). All affinity-purified antisera recognized 53bp1

Identifier	Residue	Sequence	Organism
SIGNOR-100645	Ser29	IEDSQPEsQVLEDDS	Homo sapiens
pmid	sentence
12697768	To examine whether the respective sq sites become phosphorylated in vivo, we raised polyclonal antibodies against phosphorylated ser-6 (anti-s6p), phosphorylated ser-25 and ser-29 (anti-s25p/29p), and phosphorylated ser-784 (anti-s784p). All affinity-purified antisera recognized 53bp1

Identifier	Residue	Sequence	Organism
SIGNOR-100649	Ser6	sQLDSDFS	Homo sapiens
pmid	sentence
12697768	To examine whether the respective sq sites become phosphorylated in vivo, we raised polyclonal antibodies against phosphorylated ser-6 (anti-s6p), phosphorylated ser-25 and ser-29 (anti-s25p/29p), and phosphorylated ser-784 (anti-s784p). All affinity-purified antisera recognized 53bp1

Identifier	Residue	Sequence	Organism
SIGNOR-100653	Ser784	GVEKCSDsQSWEDIA	Homo sapiens
pmid	sentence
12697768	To examine whether the respective sq sites become phosphorylated in vivo, we raised polyclonal antibodies against phosphorylated ser-6 (anti-s6p), phosphorylated ser-25 and ser-29 (anti-s25p/29p), and phosphorylated ser-784 (anti-s784p). All affinity-purified antisera recognized 53bp1

Publications:

4

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Sequence	Organism
SIGNOR-179528	Ser251	ASLQGIDsQCVNQPE	Homo sapiens
pmid	sentence
18644470	Here, we have identified two major in vitro dna-pk phosphorylation sites in the c-terminal region of xlf, serines 245 and 251. We show that these represent the major phosphorylation sites in xlf in vivo and that serine 245 is phosphorylated in vivo by dna-pk, while serine 251 is phosphorylated by ataxia-telangiectasia mutated (atm).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259942	Ser26	LRGNPSSsQVDEEQM	Homo sapiens	MiaPaCa-2 Cell
pmid	sentence
26774286	In response to ionizing radiation, ATM phosphorylates FBXW7 at serine 26 to recruit it to DNA double-strand break (DSB) sites, whereas activated DNA-PKcs phosphorylates XRCC4 at serines 325/326, which promotes binding of XRCC4 to FBXW7

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277295	Ser26	RPLIKAPsQLPLSGS	Homo sapiens	MDA-MB-231 Cell
pmid	sentence
33397932	ATM and ATR kinases phosphorylate KIFC1-S26 during DNA-damage conditions.KIFC1 was stabilized upon phosphorylation and thus promoted centrosome clustering, CIN, and tumor recurrence both in vivo and in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-73366	Ser264	EQQLFYIsQPGSSVV	Homo sapiens
pmid	sentence
10608806	In this report, we showed that atm phosphorylates a p95 peptide (ser-343) and a mre11 peptide (ser-264) in vitro, suggesting that atm may regulate the function of p95?Mre11? Rad50 repair complex in response to dna damage.

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274020	Ser27	QEENLEAsGDYKYSG	Homo sapiens	Chronic Lymphocytic Leukemia Cell
pmid	sentence
26337656	Ku70 phosphorylation occurs within minutes of genotoxic stress and involves DNA-PKcs and/or ATM kinase activities.By using specific vectors enabling the simultaneous shRNA-mediated inhibition of endogenous Ku70 and the expression of exogenous Ku70 resistant to shRNA (i.e. S27-S33-Ku70 and A27-A33-Ku70 expressing cells), we showed that phospho-Ku70 contributes to faster but error-prone DNA repair resulting in higher levels of chromosomal breaks.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274021	Ser33	ASGDYKYsGRDSLIF	Homo sapiens	Chronic Lymphocytic Leukemia Cell
pmid	sentence
26337656	Ku70 phosphorylation occurs within minutes of genotoxic stress and involves DNA-PKcs and/or ATM kinase activities.By using specific vectors enabling the simultaneous shRNA-mediated inhibition of endogenous Ku70 and the expression of exogenous Ku70 resistant to shRNA (i.e. S27-S33-Ku70 and A27-A33-Ku70 expressing cells), we showed that phospho-Ku70 contributes to faster but error-prone DNA repair resulting in higher levels of chromosomal breaks.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-105243	Ser272	LSDTDSHsQDLGSPE	Homo sapiens
pmid	sentence
11278446	Hyperphosphorylation of hrad9 induced by ir is dependent on atm. Ser(272) of hrad9 is phosphorylated directly by atm in vitro. / our results suggest that the atm-mediated phosphorylation of hrad9 is required for ir-induced checkpoint activation.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Lung

Identifier	Residue	Sequence	Organism
SIGNOR-172123	Ser274	MILIQDGsQNTNVDK	Homo sapiens
pmid	sentence
21329876	The atm kinase directly binds to and phosphorylates ksrp, leading to enhanced interaction between ksrp and pri-mirnas and increased ksrp activity in mirna processing

Identifier	Residue	Sequence	Organism
SIGNOR-172127	Ser670	GPGAPPGsQPDYSAA	Homo sapiens
pmid	sentence
21329876	The atm kinase directly binds to and phosphorylates ksrp, leading to enhanced interaction between ksrp and pri-mirnas and increased ksrp activity in mirna processing

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-78025	Ser278	VDTGITNsQTLIPDC	Homo sapiens
pmid	sentence
10839544	We have identified two residues of nbs1, ser 278 and ser 343 that are phosphorylated in vitro by atm and whose modification in vivo is essential for the cellular response to dna damage. This response includes s-phase checkpoint activation, formation of the nbs1/mrel1/rad50 nuclear foci and rescue of hypersensitivity to ionizing radiation.

Identifier	Residue	Sequence	Organism
SIGNOR-73432	Ser343	TTPGPSLsQGVSVDE	Homo sapiens
pmid	sentence
10608806	In this report, we showed that atm phosphorylates a p95 peptide (ser-343) and a mre11 peptide (ser-264) in vitro, suggesting that atm may regulate the function of p95?Mre11? Rad50 repair complex in response to dna damage.

Identifier	Residue	Sequence	Organism
SIGNOR-77149	Ser343	TTPGPSLsQGVSVDE	Homo sapiens
pmid	sentence
10802669	We show that atm physically interacts with and phosphorylates nibrin on serine 343 both in vivo and in vitro. Phosphorylation of this site appears to be functionally important because mutated nibrin (s343a) does not completely complement radiosensitivity in nbs cells.

Identifier	Residue	Sequence	Organism
SIGNOR-78030	Ser397	EQKFRMLsQDAPTVK	Homo sapiens
pmid	sentence
10839545	We have identified two residues of nbs1, ser 278 and ser 343 that are phosphorylated in vitro by atm and whose modification in vivo is essential for the cellular response to dna damage. This response includes s-phase checkpoint activation, formation of the nbs1/mrel1/rad50 nuclear foci and rescue of hypersensitivity to ionizing radiation.

Identifier	Residue	Sequence	Organism
SIGNOR-78034	Ser615	VPESSKIsQENEIGK	Homo sapiens
pmid	sentence
10839545	In vivo, nbs was phosphorylated on many serine residues, of which s343, s397 and s615 were phosphorylated by atm in vitro. Reconstituting nbs cells with a mutant form of nbs that cannot be phosphorylated at selected, atm-dependent serine residues led to a specific reduction in clonogenic survival after gamma-radiation.

Publications:

5

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-185635	Ser278	LMKFIYTsQYDNCLT	Homo sapiens	Breast Cancer Cell, Prostate Gland Cancer Cell
pmid	sentence
19412162	We find that dna damage induced by gamma-irradiation results in increased fbxo31 levels, which requires phosphorylation of fbxo31 by the ddr-initiating kinase atm

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-109416	Ser31	ALRLLDSsQIVIISA	Mus musculus
pmid	sentence
11459832	Selective induction of e2f1 in response to dna damage, mediated by atm-dependent phosphorylation. We identify a site for atm/atr phosphorylation in the amino terminus of e2f1 and we show that this site is required for atm-mediated stabilization of e2f1. Finally, we also show that e2f1 is required for dna damaged induced apoptosis in mouse thymocytes.

Publications:

1

Organism:

Mus Musculus

Pathways:

Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism
SIGNOR-177276	Ser314	SHEDLPAsQERSEVN	Homo sapiens
pmid	sentence
22099307	We also demonstrate that mitotically activated atm phosphorylates bub1, a critical kinetochore protein, on ser314. Atm-mediated bub1 ser314 phosphorylation is required for bub1 activity and is essential for the activation of the spindle checkpoint

Publications:

1

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism
SIGNOR-163106	Ser317	ENVKYSSsQPEPRTG	Homo sapiens
pmid	sentence
20068082	Atr (predominantly) or atm (to a lesser extent) phosphorylates chk1 at ser317/345, directly leading to activation.

Identifier	Residue	Sequence	Organism
SIGNOR-163110	Ser345	LVQGISFsQPTCPDH	Homo sapiens
pmid	sentence
20068082	Atr (predominantly) or atm (to a lesser extent) phosphorylates chk1 at ser317/345, directly leading to activation.

Publications:

2

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-265076	Ser318	GNSDSSSsQPLRTEN	Homo sapiens	U2-OS Cell
pmid	sentence
30612738	These results suggest that UBQLN4 phosphorylation on S318 is functionally important for its role in the DSB response.>Particularly HRR is dependent on ATM activity (Dietlein et al., 2014). Here, we showed that UBQLN4 is an ATM substrate and that DSB sealing is markedly impaired in UBQLN4-depleted cells. HRR depends on a 5′-3′ DSB end resection, which is initiated by the MRE11 nuclease

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276276	Ser337	ASGTLPVsQPKSWAS	Homo sapiens	HCT-116 Cell
pmid	sentence
20096447	The translocation and stabilization of USP10 is regulated by ATM -mediated phosphorylation of USP10 at Thr42 and Ser337.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276275	Thr42	SGTVLCGtQAVDKLP	Homo sapiens	HCT-116 Cell
pmid	sentence
20096447	The translocation and stabilization of USP10 is regulated by ATM -mediated phosphorylation of USP10 at Thr42 and Ser337.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-149292	Ser342	SKLTHSLsTSDITAI	Homo sapiens
pmid	sentence
16943424	Recently we showed that atm- and hdm2-dependent ubiquitination and subsequent degradation of hdmx following dsb induction are mediated by phosphorylation of hdmx on s403, s367, and s342, with s403 being targeted directly by atm.

Identifier	Residue	Sequence	Organism
SIGNOR-149300	Ser403	DLAHSSEsQETISSM	Homo sapiens
pmid	sentence
16943424	Recently we showed that atm- and hdm2-dependent ubiquitination and subsequent degradation of hdmx following dsb induction are mediated by phosphorylation of hdmx on s403, s367, and s342, with s403 being targeted directly by atm.

Identifier	Residue	Organism
SIGNOR-139403		Homo sapiens
pmid	sentence
16082221	Atm directly and indirectly induces mdm2 and mdmx phosphorylation, resulting in decreased activity and stability of these proteins. We recently provided a mechanism for the reduced stability of mdm2 and mdmx by showing that atm-dependent phosphorylation lowers their affinity for the deubiquitinating enzyme hausp.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-149296	Ser367	PDCRRTIsAPVVRPK	Homo sapiens
pmid	sentence
16943424	Recently we showed that atm- and hdm2-dependent ubiquitination and subsequent degradation of hdmx following dsb induction are mediated by phosphorylation of hdmx on s403, s367, and s342, with s403 being targeted directly by atm.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277534	Ser384	KILRQELsQQQPQAG	Mus musculus	MEF Cell
pmid	sentence
33097595	Using biochemical approaches and MS analysis, we show that upon the onset of the DNA-damage response, SMURF2 becomes phosphorylated at Ser384 by ataxia telangiectasia mutated (ATM) serine/threonine kinase, and this phosphorylation is required for its interaction with RNF20.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-188408	Ser386	DDKITQAsQSQESED	Homo sapiens	HEK-293 Cell
pmid	sentence
19816404	These data indicate that atm is responsible for directly phosphorylating s386 and s429 after dna damagemdm2 phosphorylation inhibits p53 poly ubiquitination

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-158324	Ser395	SQESEDYsQPSTSSS	Homo sapiens	SAOS-2 Cell
pmid	sentence
17936559	Dephosphorylation stabilizes mdm2 and increases its affinity for p53, inducing p53 degredation. ;phosphorylated s260 and s395 ands260d and s395d mutant peptides inhibited binding of binding of a specific monoclonal antibody raised to mdm2. Phosphorylation of mdm2 regulates p53 degradation.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-107256	Ser395	SQESEDYsQPSTSSS	Homo sapiens	NCI-H1299 Cell
pmid	sentence
11331603	Atm phosphorylates mdm2 on s395 in vitro. Moreover, s395 appears to be phosphorylated in an atm-dependent manner in vivo the precise mechanism through which s395 phosphorylation attenuates mdm2 function is unclear.

Identifier	Residue	Sequence	Organism
SIGNOR-94268	Ser395	SQESEDYsQPSTSSS	in vitro
pmid	sentence
12383858	Dephosphorylation stabilizes mdm2 and increases its affinity for p53, inducing p53 degredation. ;phosphorylated s260 and s395 ands260d and s395d mutant peptides inhibited binding of binding of a specific monoclonal antibody raised to mdm2. Phosphorylation of mdm2 regulates p53 degradation.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-188412	Ser429	KEESVESsLPLNAIE	Homo sapiens	HEK-293 Cell
pmid	sentence
19816404	These data indicate that atm is responsible for directly phosphorylating s386 and s429 after dna damagemdm2 phosphorylation inhibits p53 poly ubiquitination

Publications:

5

Organism:

Homo Sapiens, In Vitro

Pathways:

FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence	Organism
SIGNOR-149082	Ser387	SDDSRTAsQLDEFQE	Homo sapiens
pmid	sentence
16931761	Atm engages autodegradation of the e3 ubiquitin ligase cop1 after dna damage. We observed that in response to dna damage, atm phosphorylated cop1 on ser(387) and stimulated a rapid autodegradation mechanism

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255587	Ser404	MKGFGEYsRSPTF	Homo sapiens	HEK-293 Cell
pmid	sentence
26778126	In this study, we demonstrate that ionizing radiation (IR)-induces ATM-dependent phosphorylation of serine 404 (S404) next to the pSPxF motif. Crystal structures of BRCT/Abraxas show that phosphorylation of S404 is important for extensive interactions through the N-terminal sequence outside the pSPxF motif and leads to formation of a stable dimer.

Identifier	Residue	Sequence	Organism
SIGNOR-255588	Ser406	GPGEYSRsPTF	Homo sapiens
pmid	sentence
26778126	IR-Induced Double Phosphorylation of Abraxas C Terminus S404 and S406 Is ATM Dependent

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-265969	Ser43	RNPEAALsPTFRSDS
pmid	sentence
32615088	Here, we report that, in response to DSBs, the RNA methyltransferase METTL3 is activated by ATM-mediated phosphorylation at S43.

Publications:

1

Identifier	Residue	Sequence	Organism
SIGNOR-160648	Ser44	DEELSKKsQKWDEMN	Homo sapiens
pmid	sentence
18250156	Atm phosphorylates i-2 on serine 43, leading to the dissociation of the pp1-i-2 complex and the activation of pp1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250576	Ser440	SPLLMILsQLLPQQR	in vitro
pmid	sentence
10608806	Putative ATM in vitro targets include p95/nibrin, Mre11, Brca1, Rad17, PTS, WRN, and ATM (S440) itself.

Publications:

1

Organism:

In Vitro

Pathways:

Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Sequence
SIGNOR-275577	Ser442	IELLGMPsQKLLDAS
pmid	sentence
19965871	ATM augments nuclear stabilization of DYRK2 by inhibiting MDM2 in the apoptotic response to DNA damage\|Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus.

Identifier	Residue	Sequence
SIGNOR-275576	Thr106	NKRTVLTtQPNGLTT
pmid	sentence
19965871	ATM augments nuclear stabilization of DYRK2 by inhibiting MDM2 in the apoptotic response to DNA damage\|Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus.

Publications:

2

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-48818	Ser446	PYPGIDLsQVYELLE	Homo sapiens	Neuron
pmid	sentence
9168116	Ataxia telangiectasia mutant protein activates c-abl tyrosine kinase in response to ionizing radiation. Atm kinase domain corrects this defect, as it phosphorylates the c-abl tyrosine kinase in vitro at ser 465, leading to the activation of c-abl.

Identifier	Residue	Organism
SIGNOR-48822		Homo sapiens
pmid	sentence
9168117	Our results demonstrate that the sh3 domain of c-abl interacts with a dpapnpphfp motif (residues 1,373-1,382) of atm.These findings indicate that atm is involved in the activation of c-abl by dna damag

Publications:

2

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-265075	Ser462	DDDSDDEsQSSHTGK	Homo sapiens	U2-OS Cell
pmid	sentence
30886146	Furthermore, ATM phosphorylates UFL1 at serine 462, enhancing UFL1 E3 ligase activity and promoting ATM activation in a positive feedback loop.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-180747	Ser477	NSMNKLPsVSQLINP	Homo sapiens
pmid	sentence
18769144	Atm kinase is a master switch for the delta np63 alpha phosphorylation/degradation in human head and neck squamous cell carcinoma cells upon dna damage. We previously found that the pro-apoptotic dna damaging agent, cisplatin, mediated the proteasome-dependent degradation of delta np63 alpha associated with its increased phosphorylated status. We found that delta np63 alpha is phosphorylated in the time-dependent fashion at the following positions: s385, t397 and s466, which were surrounded by recognition motifs for atm, cdk2 and p70s6k kinases, respectively

Identifier	Residue	Sequence	Organism
SIGNOR-180751	Ser560	LARLGCSsCLDYFTT	Homo sapiens
pmid	sentence
18769144	Atm kinase is a master switch for the delta np63 alpha phosphorylation/degradation in human head and neck squamous cell carcinoma cells upon dna damage. We previously found that the pro-apoptotic dna damaging agent, cisplatin, mediated the proteasome-dependent degradation of delta np63 alpha associated with its increased phosphorylated status. We found that delta np63 alpha is phosphorylated in the time-dependent fashion at the following positions: s385, t397 and s466, which were surrounded by recognition motifs for atm, cdk2 and p70s6k kinases, respectively

Identifier	Residue	Sequence	Organism
SIGNOR-180755	Thr491	PQQRNALtPTTIPDG	Homo sapiens
pmid	sentence
18769144	Atm kinase is a master switch for the delta np63 alpha phosphorylation/degradation in human head and neck squamous cell carcinoma cells upon dna damage. We previously found that the pro-apoptotic dna damaging agent, cisplatin, mediated the proteasome-dependent degradation of delta np63 alpha associated with its increased phosphorylated status. We found that delta np63 alpha is phosphorylated in the time-dependent fashion at the following positions: s385, t397 and s466, which were surrounded by recognition motifs for atm, cdk2 and p70s6k kinases, respectively

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-137619	Ser490	QSTEPALsQIVMAPS	Homo sapiens
pmid	sentence
15916964	Here, we demonstrate that the protein kinase atm phosphorylates atf2 on serines 490 and 498 following ionizing radiation (ir). dose- and time-dependent phosphorylation of atf2 by atm that results in its rapid colocalization with gamma-h2ax and mrn components into ir-induced foci (irif)

Identifier	Residue	Sequence	Organism
SIGNOR-137623	Ser498	QIVMAPSsQSQPSGS	Homo sapiens
pmid	sentence
15916964	Here, we demonstrate that the protein kinase atm phosphorylates atf2 on serines 490 and 498 following ionizing radiation (ir). dose- and time-dependent phosphorylation of atf2 by atm that results in its rapid colocalization with gamma-h2ax and mrn components into ir-induced foci (irif)

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275854	Ser495	STSTESSsQDVESTF
pmid	sentence
31938050	Once all the three conservative SQ sites (S67, S495, and S714), in USP28, were mutated to alanine, the pS/TQ antibody completely could not recognize the immunoprecipitated Flag-USP28-3S/A (Figure Figure55D), suggesting that in response to 5'-AZA-induced stress, ATM phosphorylates USP28 at all these three sites.\|We demonstrated that the ubiquitin E3 ligase KLHL2 interacted with UCK1 and mediated its polyubiquitination at the K81 residue and degradation. We showed that deubiquitinase USP28 antagonized KLHL2-mediated polyubiquitylation of UCK1. We also provided evidence that ATM-mediated phosphorylation of USP28 resulted in its disassociation from KLHL2 and UCK1 destabilization.

Identifier	Residue	Sequence
SIGNOR-275852	Ser67	DERVKEPsQDTVATE
pmid	sentence
31938050	Once all the three conservative SQ sites (S67, S495, and S714), in USP28, were mutated to alanine, the pS/TQ antibody completely could not recognize the immunoprecipitated Flag-USP28-3S/A (Figure Figure55D), suggesting that in response to 5'-AZA-induced stress, ATM phosphorylates USP28 at all these three sites.\|We demonstrated that the ubiquitin E3 ligase KLHL2 interacted with UCK1 and mediated its polyubiquitination at the K81 residue and degradation. We showed that deubiquitinase USP28 antagonized KLHL2-mediated polyubiquitylation of UCK1. We also provided evidence that ATM-mediated phosphorylation of USP28 resulted in its disassociation from KLHL2 and UCK1 destabilization.

Identifier	Residue	Sequence
SIGNOR-275853	Ser714	ESSTNSSsQDYSTSQ
pmid	sentence
31938050	Once all the three conservative SQ sites (S67, S495, and S714), in USP28, were mutated to alanine, the pS/TQ antibody completely could not recognize the immunoprecipitated Flag-USP28-3S/A (Figure Figure55D), suggesting that in response to 5'-AZA-induced stress, ATM phosphorylates USP28 at all these three sites.\|We demonstrated that the ubiquitin E3 ligase KLHL2 interacted with UCK1 and mediated its polyubiquitination at the K81 residue and degradation. We showed that deubiquitinase USP28 antagonized KLHL2-mediated polyubiquitylation of UCK1. We also provided evidence that ATM-mediated phosphorylation of USP28 resulted in its disassociation from KLHL2 and UCK1 destabilization.

Publications:

3

Identifier	Residue	Sequence	Organism
SIGNOR-177793	Ser502	FSTDNSGsQPKQKSD	Homo sapiens
pmid	sentence
22123827	Dbf4/cdc7 (dbf4-dependent kinase (ddk)) is activated at the onset of s-phase, and its kinase activity is required for dna replication initiation from each origin. We identified novel atm/atr phosphorylation sites on dbf4 and showed that atm/atr-mediated phosphorylation of dbf4 is critical for the intra-s-phase checkpoint to inhibit dna replication.

Identifier	Residue	Sequence	Organism
SIGNOR-177797	Ser539	GLITINSsQEHLTVQ	Homo sapiens
pmid	sentence
22123827	Dbf4/cdc7 (dbf4-dependent kinase (ddk)) is activated at the onset of s-phase, and its kinase activity is required for dna replication initiation from each origin. We identified novel atm/atr phosphorylation sites on dbf4 and showed that atm/atr-mediated phosphorylation of dbf4 is critical for the intra-s-phase checkpoint to inhibit dna replication.

Identifier	Residue	Sequence	Organism
SIGNOR-177801	Thr449	DDIRQNFtQLPLHKN	Homo sapiens
pmid	sentence
22123827	Dbf4/cdc7 (dbf4-dependent kinase (ddk)) is activated at the onset of s-phase, and its kinase activity is required for dna replication initiation from each origin. We identified novel atm/atr phosphorylation sites on dbf4 and showed that atm/atr-mediated phosphorylation of dbf4 is critical for the intra-s-phase checkpoint to inhibit dna replication.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-148315	Ser503	NDEITDEsLENFPSS	Homo sapiens
pmid	sentence
16874298	The artemis nuclease is defective in radiosensitive severe combined immunodeficiency patients and is required for the repair of a subset of ionising radiation induced dna double-strand breaks (dsbs) in an atm and dna-pk dependent process. Here, we show that artemis phosphorylation by atm and dna-pk in vitro is primarily attributable to s503, s516 and s645 and demonstrate atm dependent phosphorylation at serine 645 in vivo

Identifier	Residue	Sequence	Organism
SIGNOR-148319	Ser516	SSTVAGGsQSPKLFS	Homo sapiens
pmid	sentence
16874298	The artemis nuclease is defective in radiosensitive severe combined immunodeficiency patients and is required for the repair of a subset of ionising radiation induced dna double-strand breaks (dsbs) in an atm and dna-pk dependent process. Here, we show that artemis phosphorylation by atm and dna-pk in vitro is primarily attributable to s503, s516 and s645 and demonstrate atm dependent phosphorylation at serine 645 in vivo

Identifier	Residue	Sequence	Organism
SIGNOR-148323	Ser645	NLSTNADsQSSSDFE	Homo sapiens
pmid	sentence
16874298	The artemis nuclease is defective in radiosensitive severe combined immunodeficiency patients and is required for the repair of a subset of ionising radiation induced dna double-strand breaks (dsbs) in an atm and dna-pk dependent process. Here, we show that artemis phosphorylation by atm and dna-pk in vitro is primarily attributable to s503, s516 and s645 and demonstrate atm dependent phosphorylation at serine 645 in vivo

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276318	Ser520	CRADELAsQDGR	Homo sapiens	U2-OS Cell
pmid	sentence
21460856	In the present study, we demonstrate that ataxia-telangiectasia mutated (ATM) directly phosphorylates and specifically regulates B56γ3, B56γ2 and B56δ, after DNA damage. We further show that phosphorylation of B56γ3 at Ser510 leads to an increase in B56γ3-PP2A complexes, and direction of PP2A phosphatase activity toward the substrate p53, activating its tumor-suppressive functions. we show that Ser510 phosphorylation significantly enhances the ability of B56γ3 to inhibit cell proliferation and anchorage-independent growth.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-126308	Ser535	ATDDPNFsQEDQQDT	Homo sapiens
pmid	sentence
15210935	Atm phosphorylates mcm3 on s535 in response to ionizing radiation. Second, atr phosphorylates mcm2 on s108 in response to multiple forms of dna damage and stalling of replication forksthe functional consequences of mcm2 s108 and mcm3 s535 phosphorylation are not clear

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-200889	Ser564	LEEESPVsQLFELEI	Homo sapiens
pmid	sentence
23405218	The main phosphorylation site of daxx is identified to be ser564, which is a direct target of atm. Phosphorylation of endogenous daxx at ser564 occurs rapidly during the dna damage response and precedes p53 activation. Blockage of this phosphorylation event prevents the separation of daxx from mdm2, stabilizes mdm2, and inhibits dna damage-induced p53 activation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-156077	Ser635	KLFDVCGsQDFESDL	Homo sapiens
pmid	sentence
17570479	The ms/ms fragmentation spectra (figure s7) confirmed the phosphorylation of rad50 at the predicted atm substrate site, s635, in agreement with published data

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273511	Ser64	PVAGSAVsQELREGD	Homo sapiens	U2-OS Cell
pmid	sentence
27715493	Here, we show that in response to various types of DNA damage, including IR and UV, WRAP53β is phosphorylated on serine residue 64 by ATM with a time-course that parallels its accumulation at DNA lesions. Interestingly, recruitment of phosphorylated WRAP53β (pWRAP53βS64) to sites of such DNA damage promotes its interaction with γH2AX at these locations.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-73520	Ser646	ETWSLPLsQNSASEL	Homo sapiens
pmid	sentence
10608806	We determined a general phosphorylation consensus sequence for atm and identified putative in vitro targets by using glutathione s-transferase peptides as substrates. Putative atm in vitro targets include p95/nibrin, mre11, brca1, rad17, pts, wrn, and atm (s440) itself.

Identifier	Residue	Sequence	Organism
SIGNOR-73524	Ser656	SASELPAsQPQPFSA	Homo sapiens
pmid	sentence
10608806	We determined a general phosphorylation consensus sequence for atm and identified putative in vitro targets by using glutathione s-transferase peptides as substrates. Putative atm in vitro targets include p95/nibrin, mre11, brca1, rad17, pts, wrn, and atm (s440) itself.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-79872	Ser664	IDPGADLsQYKMDVT	Homo sapiens	Breast Cancer Cell
pmid	sentence
10910365	Atm phosphorylates ctip at serine residues 664 and 745 our study suggests another dna damage-response pathway in which the signal is transmitted through phosphorylation of ctip by atm, leading to dissociation of the ctip_ctbp repressor complex from brca1, which in turn, activate transcription of gadd45

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-79876	Ser745	SCLADSFsQAADEEE	Homo sapiens	Breast Cancer Cell
pmid	sentence
10910365	Atm phosphorylates ctip at serine residues 664 and 745 our study suggests another dna damage-response pathway in which the signal is transmitted through phosphorylation of ctip by atm, leading to dissociation of the ctip_ctbp repressor complex from brca1, which in turn, activate transcription of gadd45

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277307	Ser677	RVGKQLAsQKILQLL	Homo sapiens	HEK-293T Cell
pmid	sentence
34188037	Specifically, radiation-induced ATM-dependent phosphorylation of DGCR8 at serine 677 facilitates USP51 to bind, deubiquitinate, and stabilize DGCR8, which leads to the recruitment of DGCR8 and DGCR8's binding partner RNF168 to MDC1 and RNF8 at DSBs.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273513	Ser68	NTYETELsQWEMSDR	Homo sapiens	HCT-116 Cell
pmid	sentence
19377469	These results indicate that Apak is a genuine substrate of ATM kinase. Apak phosphorylation on Ser 68 is critical for p53-mediated apoptosis. in response to DNA damage, ATM is rapidly activated by autophosphorylation and mediates p53 activation through disruption of the Apak–p53 complex by phosphorylating Apak on Ser 68.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-169999	Ser696	NVLSVALsQRTTVPE	Homo sapiens
pmid	sentence
21095582	Here we show that hypoxia results in ataxia telangiectasia mutated (atm)-dependent phosphorylation of hypoxia-inducible factor 1-alpha (hif-1_) on serine(696) and mediates downregulation of mtorc1 signaling. phosphorylation of hif-1_ by atm is required for its stability

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-182423	Ser72	TAEEVDLsKDLPHWN	Homo sapiens
pmid	sentence
19015526	Atm-mediated serine 72 phosphorylation stabilizes ribonucleotide reductase small subunit p53r2 protein against mdm2 to dna damage

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-276602	Ser729	LFFDYRYsQADALKY	in vitro
pmid	sentence
24162653	Enhancer of zeste homolog 2 (EZH2), a core catalytic component of PRC2, is a new ATM kinase target, and ATM-mediated phosphorylation of EZH2 on Ser734 reduces protein stability.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255590	Ser730	LDKSADFsQSTSIGI	Homo sapiens	HEK-293 Cell
pmid	sentence
17412408	Three phosphorylation sites were detected in a human KIAA1794 protein: S730, T952, S1121, and two other sites in the mouse protein S555, T558. We renamed the KIAA1794 protein as FANCI, since, as shown below, the locus encoding this protein is mutated in an individual with Fanconi anemia complementation group I

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275798	Ser74	EFEELTMsQKNGGNV
pmid	sentence
27879648	Deoxycytidine kinase (dCK) is a key enzyme in deoxyribonucleoside salvage and the anti-tumor activity for many nucleoside analogs. dCK is activated in response to ionizing radiation (IR)-induced DNA damage and it is phosphorylated on Serine 74 by the Ataxia-Telangiectasia Mutated (ATM) kinase in order to activate the cell cycle G2/M checkpoint.

Publications:

1

Identifier	Residue	Sequence
SIGNOR-275910	Ser75	EEEEKIKsQGQDVTS
pmid	sentence
27941124	The deubiquitinase UCHL3 is phosphorylated and activated by ATM. UCHL3, in turn, deubiquitinates RAD51 and promotes the binding between RAD51 and BRCA2. \|Mutation of S75 (S75A) abolished the pSQ/TQ signal, suggesting that S75 is a major ATM phosphorylation site following DNA damage

Publications:

1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-183454	Ser794	LSNCTKKsPNKIASG	Homo sapiens	Neuron
pmid	sentence
19151707	Here we show that cdk5 (cyclin-dependent kinase 5), activated by dna damage, directly phosphorylates atm at ser 794 in post-mitotic neurons. Phosphorylation at ser 794 precedes, and is required for, atm autophosphorylation at ser 1981, and activates atm kinase activity

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-188772	Ser81	PKRQKSGsQEDLGWC	Homo sapiens
pmid	sentence
19851285	Optimal function of the dna repair enzyme tdp1 requires its phosphorylation by atm and/or dna-pk. Here we show that top1-associated dna double-stranded breaks (dsbs) induce the phosphorylation of tdp1 at s81. This phosphorylation is mediated by the protein kinases: ataxia-telangiectasia-mutated (atm) and dna-dependent protein kinase (dna-pk)

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-144813	Ser85	ELLHFQAsQREEKEF	Homo sapiens
pmid	sentence
16497931	Atm phosphorylates serine-85 of nemo to promote its ubiquitin-dependent nuclear export.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-115492	Ser957	ISQEEGSsQGEDSVS	Homo sapiens
pmid	sentence
11877377	Here we report that smc1 is a component of the dna damage response network that functions as an effector in the atm/nbs1-dependent s-phase checkpoint pathway. Smc1 associates with brca1 and is phosphorylated in response to ir in an atm- and nbs1-dependent manner. Using mass spectrometry, we established that atm phosphorylates s957 and s966 of smc1 in vivo.

Identifier	Residue	Sequence	Organism
SIGNOR-115496	Ser966	GEDSVSGsQRISSIY	Homo sapiens
pmid	sentence
11877377	Here we report that smc1 is a component of the dna damage response network that functions as an effector in the atm/nbs1-dependent s-phase checkpoint pathway. Smc1 associates with brca1 and is phosphorylated in response to ir in an atm- and nbs1-dependent manner. Using mass spectrometry, we established that atm phosphorylates s957 and s966 of smc1 in vivo.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255589	Ser966	GEDSVSGsQRISSIY	Homo sapiens	GM0536 Cell
pmid	sentence
11877376	Atm phosphorylates Smc1 on serines 957 and 966 in vitro and in vivo, and expression of an Smc1 protein mutated at these phosphorylation sites abrogates the ionizing irradiation-induced S phase cell cycle checkpoint

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-124043	Ser97	TIAESEDsQESVDSV	Homo sapiens
pmid	sentence
15073328	Individual ala substitutions at thr-100, ser-111, or ser-121 inhibited atm-catalyzed phosphate incorporationatm phosphorylated creb in vitro and in vivophosphorylation of creb correlated with a decrease in creb transactivation potential and reduced interaction between creb and its transcriptional coactivator, creb-binding protein (cbp)

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism
SIGNOR-154167	Ser990	SRSTSVTsQISNGSH	Homo sapiens
pmid	sentence
17396146	The dna damage kinase ataxia telangiectasia mutated (atm) phosphorylates taos in vitro;radiation induces phosphorylation of tao on a consensus site for phosphorylation by the atmprotein kinase in cells.

Identifier	Residue	Sequence	Organism
SIGNOR-154171	Thr643	EELNKRQtQKDLEHA	Homo sapiens
pmid	sentence
17396146	The dna damage kinase ataxia telangiectasia mutated (atm) phosphorylates taos in vitro;radiation induces phosphorylation of tao on a consensus site for phosphorylation by the atmprotein kinase in cells.

Identifier	Residue	Sequence	Organism
SIGNOR-154175	Thr785	SINEMLStQALRLDE	Homo sapiens
pmid	sentence
17396146	The dna damage kinase ataxia telangiectasia mutated (atm) phosphorylates taos in vitro;radiation induces phosphorylation of tao on a consensus site for phosphorylation by the atmprotein kinase in cells.

Identifier	Residue	Organism
SIGNOR-154178		Homo sapiens
pmid	sentence
17396146	The dna damage kinase ataxia telangiectasia mutated (atm) phosphorylates taos in vitro;radiation induces phosphorylation of tao on a consensus site for phosphorylation by the atmprotein kinase in cells.

Publications:

4

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262639	Thr117	EPNPEYStQQAPNKA	Mus musculus	Foreskin Fibroblast Cell Line
pmid	sentence
18449195	Ataxia telangiectasia mutated (ATM) kinase phosphorylates hSSB1 in response to DNA double-strand breaks (DSBs). This phosphorylation event is required for DNA damage-induced stabilization of hSSB1.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276499	Thr134	SRAAFSHtQVIELER	Homo sapiens	HEK-293T Cell
pmid	sentence
23890999	ATM phosphorylates NKX3.1 on T166 and then T134, resulting in NKX3.1 ubiquitination and degradation resulting from an apparent regulatory interaction.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276500	Thr166	KNLKLTEtQVKIWFQ	Homo sapiens	HEK-293T Cell
pmid	sentence
23890999	ATM phosphorylates NKX3.1 on T166 and then T134, resulting in NKX3.1 ubiquitination and degradation resulting from an apparent regulatory interaction.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273505	Thr145	IEVREAGtQRSVEVR	Homo sapiens	Embryonic Stem Cell
pmid	sentence
31609975	Notably, we identified two critical residues, Thr145 and Thr156, whose phosphorylation by Ataxia-telangiectasia mutated (ATM) is essential for KHDC3L's functions.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273504	Thr156	VEVREAGtQRSVEVQ	Homo sapiens	Embryonic Stem Cell
pmid	sentence
31609975	Notably, we identified two critical residues, Thr145 and Thr156, whose phosphorylation by Ataxia-telangiectasia mutated (ATM) is essential for KHDC3L's functions.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275488	Thr172	SDGEFLRtSCGSPNY
pmid	sentence
23871434	ATM phosphorylates AMPKalpha2 to induce inhibitory phosphorylation of HIPK2\|

Publications:

1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273836	Thr204	EASDGEEtQVSAADL	Homo sapiens	HEK-293 Cell
pmid	sentence
28109743	We show that Polλ is efficiently phosphorylated by DNA-PKcs in vitro and predominantly by ATM after DSB induction with ionizing radiation (IR) in vivo. We identify threonine 204 (T204) as a main target for ATM/DNA-PKcs phosphorylation on human Polλ, and establish that its phosphorylation may facilitate the repair of a subset of IR-induced DSBs and the efficient Polλ-mediated gap-filling during NHEJ.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273510	Thr204	EASDGEEtQVSAADL	Homo sapiens	HEK-293 Cell
pmid	sentence
28109743	We identify threonine 204 (T204) as a main target for ATM/DNA-PKcs phosphorylation on human Polλ, and establish that its phosphorylation may facilitate the repair of a subset of IR-induced DSBs and the efficient Polλ-mediated gap-filling during NHEJ.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-121865	Thr21	YGGAGGYtQSPGGFG	Homo sapiens
pmid	sentence
14872059	Atm and dna?PK Phosphorylate rpa32 thr21in vitro and in vivo

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-121861	Thr21	YGGAGGYtQSPGGFG	Homo sapiens
pmid	sentence
14872059	Replication protein a (rpa) is a single-stranded dna (ssdna) binding protein involved in various processes, including nucleotide excision repair and dna replication. The 32 kda subunit of rpa (rpa32) is phosphorylated in response to various dna-damaging agents, and two protein kinases, ataxia-telangiectasia mutated (atm) and the dna-dependent protein kinase (dna-pk) have been implicated in dna damage-induced phosphorylation of rpa32we show that both dna-pk and atm phosphorylate rpa32 on thr21 in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-151441	Thr2609	LTPMFVEtQASQGTL	Homo sapiens
pmid	sentence
17189255	Atm mediates dna-pkcs phosphorylation at thr-2609 as well as at the adjacent (s/t)q motifs within the thr-2609 cluster. In addition, our data suggest that dna-pkcs- and atm-mediated dna-pkcs phosphorylations are cooperative and required for the full activation of dna-pkcs and the subsequent dsb repair.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-92877	Thr363	IEDDIIYtQDFTVPG	Homo sapiens	Melanoma Cell
pmid	sentence
12234250	We demonstrate that both dna-pk and atm efficiently phosphorylate lkb1 at thr-366 in vitro and provide evidence that atm mediates this phosphorylation in vivo. however, phosphorylation of lkb1 at thr-366 may have some role in enabling lkb1 to suppress cell growth

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-92873	Thr367	IIYTQDFtVPGQVPE	Homo sapiens	Melanoma Cell
pmid	sentence
12234250	We demonstrate that both dna-pk and atm efficiently phosphorylate lkb1 at thr-366 in vitro and provide evidence that atm mediates this phosphorylation in vivo.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-199276	Thr434	TPPPSPNtQTPVQPP	Homo sapiens	Lung Cancer Cell
pmid	sentence
23108047	Phosphorylation of ccdc6 at thr434 by atm during dna damage response prevents fbxw7-mediated ccdc6 degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275580	Thr440	ANREECRtQEKVNAT
pmid	sentence
32726637	Altogether, the results suggest that ATM-mediated T440 phosphorylation enhances LARP7-BARD1 interaction and facilitates BRCA1/BARD1-mediated LARP7 ubiquitination and degradation.

Publications:

1

Identifier	Residue	Sequence	Organism
SIGNOR-267661	Thr454	AAEAAPPtQEAQGET	Homo sapiens
pmid	sentence
22735644	Here, we report that, in human cell lines, DNA damage triggered the phosphorylation of DBC1 on Thr454 by ATM (ataxia telangiectasia-mutated) and ATR (ataxia telangiectasia and Rad3-related) kinases. Phosphorylated DBC1 bound to and inhibited SIRT1, resulting in the dissociation of the SIRT1-p53 complex and stimulating p53 acetylation and p53-dependent cell death.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262640	Thr788	DAETGFLtQSNLLSV	Homo sapiens	HeLa Cell
pmid	sentence
22854598	ATM phosphorylates PIDD on Thr788 within the DD. This phosphorylation is necessary and sufficient for RAIDD binding and caspase-2 activation. Conversely, nonphosphorylatable PIDD fails to bind RAIDD or activate caspase-2, and engages prosurvival RIP1 instead. Thus, ATM phosphorylation of the PIDD DD enables a binary switch through which cells elect to survive or die upon DNA injury.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-88010	Thr99	NAPAGQEtQRGGSKS	Homo sapiens
pmid	sentence
12034743	Mitotic phosphorylation of blm was partially dependent on atm, and phosphorylation sites on blm were identified. A phosphospecific antibody against one of these sites (thr-99) revealed radiation-induced phosphorylation, which was defective in ataxia-telangiectasia cells. These data suggest that atm and blm function together in recognizing abnormal dna structures by direct interaction and that these phosphorylation sites in blm are important for radiosensitivity status but not for sce frequency.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-276872	Tyr370	SLEISQSyTTTQRES	in vitro
pmid	sentence
25601159	Here, we show that upon irradiation stimulation, ATM associates with and is phosphorylated by epidermal growth factor receptor (EGFR) at Tyr370 (Y370) at the site of DNA double-strand breaks.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-262791		Homo sapiens	HEK-293 Cell
pmid	sentence
26344566	We report that the PEX5 peroxisome import receptor binds ataxia-telangiectasia mutated (ATM) and localizes this kinase to the peroxisome. In response to ROS, ATM signalling activates ULK1 and inhibits mTORC1 to induce autophagy.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-98798		Homo sapiens
pmid	sentence
12607003	We show that, in response to ionizing radiation, mdc1 is hyperphosphorylated in an atm-dependent manner, and rapidly relocalizes to nuclear foci that also contain the mre11 complex, phosphorylated histone h2ax and 53bp1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-65966		Homo sapiens
pmid	sentence
10097108	Atm also contributes to the cdc25c activity, particularly in ir-damaged cells, by activating chk2.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-277158		Homo sapiens
pmid	sentence
22361354	After ionizing radiation, dephosphorylation of USP7S by the ATM-dependent protein phosphatase PPM1G leads to USP7S downregulation, followed by Mdm2 downregulation and accumulation of p53. \|ATM Dependent Downregulation of USP7 and HAUSP by PPM1G Activates p53 Response to DNA Damage.\|DNA Damage Leads to ATM Dependent USP7S Dephosphorylation by PPM1G.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255511		Homo sapiens	HGC-27 Cell
pmid	sentence
19051271	we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-276320		Homo sapiens	U2-OS Cell
pmid	sentence
21460856	In the present study, we demonstrate that ataxia-telangiectasia mutated (ATM) directly phosphorylates and specifically regulates B56γ3, B56γ2 and B56δ, after DNA damage. We further show that phosphorylation of B56γ3 at Ser510 leads to an increase in B56γ3-PP2A complexes, and direction of PP2A phosphatase activity toward the substrate p53, activating its tumor-suppressive functions. we show that Ser510 phosphorylation significantly enhances the ability of B56γ3 to inhibit cell proliferation and anchorage-independent growth.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-198473		Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
22832221	Brca1/e2f1/ctipbinding to atm promoter activates atm transcription.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-253948		Homo sapiens	Pancreatic Cancer Cell
pmid	sentence
17312387	In contrast, BTF3 silencing resulted in down-regulation of several cancer-associated genes, including EPHB2, ABL2, HPSE2 and ATM, and up-regulation of KRAG, RRAS2, NFkappa-B, MRVI1, MADCAM1 and others. In conclusion, BTF3 is overexpressed in PDAC, where it acts as a transcriptional regulator rather than a direct modulator of apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-175003		Homo sapiens
pmid	sentence
21763684	E3 ubiquitin ligase, a heterodimeric complex of the ringfinger rfn20/rfn40 is phosphorylated by atm.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-193600		Homo sapiens
pmid	sentence
Other

Identifier	Residue	Organism
SIGNOR-132441		Homo sapiens
pmid	sentence
15604286	Through screening a small molecule compound library developed for the phosphatidylinositol 3'-kinase-like kinase family, we identified an atp-competitive inhibitor, 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one (ku-55933), that inhibits atm with an ic(50) of 13 nmol/l and a ki of 2.2 nmol/l

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-175053		Homo sapiens
pmid	sentence
21763684	One of the earliest events is recruitment and activation of the atm at the damaged dna sites through the mre11rad50nbs1 (mrn) sensor complex. . the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm kinase.

Identifier	Residue	Organism
SIGNOR-181634		Homo sapiens
pmid	sentence
18854157	One of the earliest events is recruitment and activation of the atm at the damaged dna sites through the mre11rad50nbs1 (mrn) sensor complex. . the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm kinase.

Publications:

2

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Organism
SIGNOR-261975		in vitro
pmid	sentence
18794134	A targeted compound library was screened for potential inhibitors of the ATM kinase, and CP466722 was identified.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-198470		Homo sapiens
pmid	sentence
22832221	Brca1/e2f1/ctipbinding to atm promoter activates atm transcription.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263323
pmid	sentence
18680434	It is not yet clear how the presence of TRF2 at telomeres averts the activation of the ATM kinase.> In this regard, overexpression of TRF2can dampen the activation of the ATM kinase, even at nontelomeric sites of DNA damage (95). Furthermore, TRF2 can interact with the ATM kinase as well as with the Mre11 complex

Publications:

1

Identifier	Residue	Organism
SIGNOR-259059		Homo sapiens
pmid	sentence
15342490	Human Rif1, ortholog of a yeast telomeric protein, is regulated by ATM and 53BP1 and functions in the S-phase checkpoint. After induction of double-strand breaks (DSBs), Rif1 formed foci that colocalized with other DNA-damage-response factors. This response was strictly dependent on ATM (ataxia telangiectasia mutated) and 53BP1, but not affected by diminished function of ATR (ATM- and Rad3-related kinase), BRCA1, Chk2, Nbs1, and Mre11.

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Organism
SIGNOR-134508		Homo sapiens
pmid	sentence
15758953	Nbs1 can also immobilize atm at the site of the dsb via direct binding of atm to a c-terminal atm interaction motif on nbs1 . the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm

Identifier	Residue	Organism
SIGNOR-181631		Homo sapiens
pmid	sentence
18854157	Nbs1 can also immobilize atm at the site of the dsb via direct binding of atm to a c-terminal atm interaction motif on nbs1 . the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-242612		Homo sapiens
pmid	sentence
21034966	the ATM-Chk2 and ATR-Chk1 pathways, which are activated by DNA double-strand breaks (DSBs) and single-stranded DNA respectively.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Organism
SIGNOR-181628		Homo sapiens
pmid	sentence
18854157	One of the earliest events is recruitment and activation of the atm at the damaged dna sites through the mre11rad50nbs1 (mrn) sensor complex. the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm kinase.

Identifier	Residue	Organism
SIGNOR-175006		Homo sapiens
pmid	sentence
21763684	One of the earliest events is recruitment and activation of the atm at the damaged dna sites through the mre11rad50nbs1 (mrn) sensor complex. the mre11/rad50/nbs1 (mrn) complex maintains genomic stability by bridging dna ends and initiating dna damage signaling through activation of the atm kinase.

Publications:

2

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-265073		Homo sapiens	HEK-293 Cell
pmid	sentence
30886146	UFM1 specific ligase 1 (UFL1), an ufmylation E3 ligase, is important for ATM activation. UFL1 is recruited to double strand breaks by the MRE11/RAD50/NBS1 complex, and monoufmylates histone H4 following DNA damage.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-174949		Homo sapiens
pmid	sentence
21763684	E3 ubiquitin ligase, a heterodimeric complex of the ringfinger rfn20/rfn40 is phosphorylated by atm.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-262536		Homo sapiens	SH-SY5Y Cell
pmid	sentence
28341201	KU-55933 blocked phosphorylation of ATM in H2O2 and Dox models of cell damage. the neuroprotective efficacy of KU-55933, a potent inhibitor of ATM, against cell damage evoked by oxidative stress (hydrogen peroxide, H2O2) has been studied in human neuroblastoma SH-SY5Y cells and compared with the efficacy of this agent in models of doxorubicin (Dox)- and staurosporine (St)-evoked cell death.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-255499		Homo sapiens	HGC-27 Cell
pmid	sentence
19051271	we performed microarray analysis to compare the gene expression profiles in HGC-27 cells, with or without small interfering RNA (siRNA)-mediated depletion of TWIST. Our results showed that NF1, RAP1A, SRPX, RBL2, PFDN4, ILK, F2R, ERBB3, and MYB were up-regulated, whereas AKR1C2, FOS, GDF15, NR2F1, ATM, and CTPS were down-regulated after TWIST depletion

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-191094		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244392		Homo sapiens
pmid	sentence
18534819	The decreased atm expression suggests that atm is involved in the development of insulin resistance through down-regulation of akt activity.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Muscle

Pathways:

FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition

Identifier	Residue	Organism
SIGNOR-185135		Homo sapiens
pmid	sentence
19360021	The negative regulator wip1 plays an important role in inhibiting atm, resulting in a pulse of atm activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-253376		Homo sapiens	HEK-293 Cell
pmid	sentence
12556884	Cellular irradiation induces rapid intermolecular autophosphorylation of serine 1981 that causes dimer dissociation and initiates cellular ATM kinase activity. Most ATM molecules in the cell are rapidly phosphorylated on this site after doses of radiation as low as 0.5 Gy, and binding of a phosphospecific antibody is detectable after the introduction of only a few DNA double-strand breaks in the cell. Activation of the ATM kinase seems to be an initiating event in cellular responses to irradiation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer

Identifier	Residue	Organism
SIGNOR-193597		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-160644		Homo sapiens
pmid	sentence
18250156	Furthermore, atm-mediated i-2 phosphorylation results in the inhibition of the aurora-b kinase, the down-regulation of histone h3 serine 10 phosphorylation, and the activation of the g2/m checkpoint.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263322
pmid	sentence
18680434	It is not yet clear how the presence of TRF2 at telomeres averts the activation of the ATM kinase.> In this regard, overexpression of TRF2can dampen the activation of the ATM kinase, even at nontelomeric sites of DNA damage (95). Furthermore, TRF2 can interact with the ATM kinase as well as with the Mre11 complex

Publications:

1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-275963
pmid	sentence
31938050	ATM also phosphorylates UCK1 at S145, significantly enhancing the KLHL2-UCK1 complex formation\|We demonstrated that the ubiquitin E3 ligase KLHL2 interacted with UCK1 and mediated its polyubiquitination at the K81 residue and degradation.

Publications:

1

Identifier	Residue	Organism	Cell Line
SIGNOR-198467		Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
22832221	Brca1/e2f1/ctipbinding to atm promoter activates atm transcription.

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer, Cell cycle: G2/M phase transition

Identifier	Residue	Organism
SIGNOR-262638		in vitro
pmid	sentence
18571408	These data suggest that Aven overexpression can activate ATM and that Aven phosphorylation in a positive feedback loop enforces Aven activity, making it a more potent ATM activator.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-276319		Homo sapiens	U2-OS Cell
pmid	sentence
21460856	In the present study, we demonstrate that ataxia-telangiectasia mutated (ATM) directly phosphorylates and specifically regulates B56γ3, B56γ2 and B56δ, after DNA damage. We further show that phosphorylation of B56γ3 at Ser510 leads to an increase in B56γ3-PP2A complexes, and direction of PP2A phosphatase activity toward the substrate p53, activating its tumor-suppressive functions. we show that Ser510 phosphorylation significantly enhances the ability of B56γ3 to inhibit cell proliferation and anchorage-independent growth.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-162304		Homo sapiens
pmid	sentence
20019063	The phosphorylation of exo1 by atm appears to regulate the activity of exo1 following resection, allowing optimal rad51 loading and the completion of hr repair.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-266785		Homo sapiens
pmid	sentence
31225475	L3MBTL2 links RNF8 and RNF168 in the DNA double strand break response. The protein kinase ATM phosphorylates L3MBTL2, which recruits it to the DNA lesion by promoting the interaction between MDC1 and L3MBTL2. L3MBTL2 is subsequently ubiquitinated by RNF8, which acts as a docking site for RNF168, thereby recruiting the ubiquitin ligase to the damage site. RNF168, in turn, ubiquitinates H2A-type histones to amplify the DNA damage response and recruit downstream DNA repair proteins for proper DSB signaling.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-161434		Homo sapiens
pmid	sentence
18534819	The decreased atm expression suggests that atm is involved in the development of insulin resistance through down-regulation of akt activity.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Muscle

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-253927		Homo sapiens	Natural Killer Cell
pmid	sentence
21406724	The up-regulation of PVR expression involves DNA-damage response (DDR)-dependent pathways, because we found that pharmacologic inhibition of ATM and ATR kinases reduced PVR expression and that PVR was almost exclusively induced on cells expressing the DDR marker γH2AX.

Publications:

1

Organism:

Homo Sapiens

Name	ATM View Modifications
Full Name	Serine-protein kinase ATM
Synonyms	Ataxia telangiectasia mutated, A-T mutated
Primary ID	Q13315
Links	- -
Type	protein
Relations	241
Pathways	Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Myogenesis modulation: DNA damage, p53 in cancer, Satellite: DDR inhibition
Inhibitors	2-(4-morpholinyl)-6-(1-thianthrenyl)-4-pyranone; 2-(6,7-dimethoxy-4-quinazolinyl)-5-(2-pyridinyl)-1,2,4-triazol-3-amine; KU-55933; KU-60019
Function	Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, UFL1, RAD9, UBQLN4 and DCLRE1C (PubMed:9843217, PubMed:9733515, PubMed:10550055, PubMed:10766245, PubMed:10839545, PubMed:10910365, PubMed:10802669, PubMed:10973490, PubMed:11375976, PubMed:12086603, PubMed:15456891, PubMed:19965871, PubMed:30612738, PubMed:30886146). May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response. Phosphorylates ERCC6 which is essential for its chromatin remodeling activity at DNA double-strand breaks (PubMed:29203878).

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