Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-124060	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 potentialit is, therefore, likely that atm and atr regulate creb phosphorylation collectively in response to stress stimuli.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism
SIGNOR-126363	Ser108	DVEELTAsQREAAER	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	Cell Line
SIGNOR-277187	Ser1141	PEKAYSSsQPVISAQ	Homo sapiens	HeLa Cell
pmid	sentence
26695548	A serine residue, S1141, in WRN is phosphorylated in vivo by the ATR kinase in response to replication stress. ATR-mediated WRN S1141 phosphorylation leads to ubiquitination of WRN, facilitating the reversible interaction of WRN with perturbed replication forks and subsequent degradation of WRN.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250581	Ser1143	PMGSSHAsQVCSETP	Homo sapiens	HEK-293T Cell
pmid	sentence
11114888	Of the four potential phosphoacceptor sites in the BRCA1 (1005–1313) fragment (Ser 1143, Ser 1239, Ser 1280, Ser 1298), Ala substitutions at two sites, Ser 1143 and Ser 1280, reduced the in vitro phosphorylation of GST–BRCA1 (1005–1313) by ATR, whereas substitution of Ser 1239 or Ser 1298 with Ala had little or no effect (Fig. 2C; data not shown). A Ser 1143/Ser 1280 double mutant was a poor substrate for ATR, suggesting that these are the two major in vitro phosphorylation sites on this BRCA1 fragment. \| Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250582	Ser1280	QVILAKAsQEHHLSE	Homo sapiens	HEK-293T Cell
pmid	sentence
11114888	Of the four potential phosphoacceptor sites in the BRCA1 (1005–1313) fragment (Ser 1143, Ser 1239, Ser 1280, Ser 1298), Ala substitutions at two sites, Ser 1143 and Ser 1280, reduced the in vitro phosphorylation of GST–BRCA1 (1005–1313) by ATR, whereas substitution of Ser 1239 or Ser 1298 with Ala had little or no effect (Fig. 2C; data not shown). A Ser 1143/Ser 1280 double mutant was a poor substrate for ATR, suggesting that these are the two major in vitro phosphorylation sites on this BRCA1 fragment. \| Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-106432	Ser1387	EDCSGLSsQSDILTT	Homo sapiens	Lymphoblastoid Cell Line
pmid	sentence
11278964	Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-106436	Ser1423	AVLEQHGsQPSNSYP	Homo sapiens	Lymphoblastoid Cell Line
pmid	sentence
11278964	Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-106440	Ser1457	SEKAVLTsQKSSEYP	Homo sapiens	Lymphoblastoid Cell Line
pmid	sentence
11278964	Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250583	Thr1394	SQSDILTtQQRDTMQ	Homo sapiens	HEK-293T Cell
pmid	sentence
11114888	Although no single mutation eliminated the GST–BRCA1 (1314–1863) electrophoretic mobility shift, a quadruple mutant (GST–BRCA14A) containing Ala substitutions at Ser 1387, Thr 1394, Ser 1423, and Ser 1457 showed no alteration in electrophoretic mobility after phosphorylation by ATR-containing immune complexes (Fig.2D). The total incorporation of 32Pi into the GST–BRCA14Asubstrate was reduced by 70% relative to that obtained with wild-type GST–BRCA1 (1314–1863), suggesting that these four residues account for most, but not all of the phosphorylation sites in this fragment. \| Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication.

Publications:

6

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273514	Ser118	SELRSELsQSQHEVN	Homo sapiens	HCT-116 Cell
pmid	sentence
21779472	MCC is phosphorylated at the ATM/ATR consensus sites Ser118 and Ser120. Finally, mutation of S118/120 to alanine did not affect MCC nuclear shuttling following UV but did impair MCC G2/M checkpoint activity.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273515	Ser120	LRSELSQsQHEVNED	Homo sapiens	HCT-116 Cell
pmid	sentence
21779472	MCC is phosphorylated at the ATM/ATR consensus sites Ser118 and Ser120. Finally, mutation of S118/120 to alanine did not affect MCC nuclear shuttling following UV but did impair MCC G2/M checkpoint activity.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-182953	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
SIGNOR-115134	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
11865061	Nhibition of atr kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on serine 15 as well as p53 protein accumulation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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-250584	Ser173	VKKNPHHsQWGDMKL	Homo sapiens	A-549 Cell
pmid	sentence
16540648	Defects in ATR-dependent XPA phosphorylation increases the cell sensitivity to UV irradiation. \| The XPA-deficient cells complemented with XPA-S196A mutant, in which Ser196 was substituted with an alanine, displayed significantly higher UV sensitivity compared with the XPA cells complemented with wild-type XPA. Moreover, substitution of Ser196 with aspartic acid for mimicking the phosphorylation of XPA increased the cell survival to UV irradiation.

Identifier	Residue	Sequence	Organism
SIGNOR-258985	Ser196	RSLEVWGsQEALEEA	Homo sapiens
pmid	sentence
30327428	ATR mediated phosphorylation of XPA on S196 enhances cAMP-mediated optimization of NER, and is promoted by SIRT1-mediated deacetylation of XPA on K63, K67 and K215.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277551	Ser179	FRPEYSAsQLKGFSL	Homo sapiens	A-549 Cell
pmid	sentence
33811702	Specifically, ATR binds to and phosphorylates PARP1 at Ser179 after the ionophore treatments. This site-specific phosphorylation inactivates PARP1, inhibiting ionophore-induced necrosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276167	Ser19	GTSKCPPsQRVPALT	Homo sapiens	HEK-293T Cell
pmid	sentence
18536714	We have also demonstrated that DNA damage triggers disruption of the HIPK2-Siah-1 complex, resulting in HIPK2 stabilization and activation. 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-199802	Ser196	RSLEVWGsQEALEEA	Homo sapiens
pmid	sentence
23178497	Atr phosphorylates xpa. at serine 196. Atr-mediated xpa phosphorylation enhances xpa stability by inhibiting herc2-mediated ubiquitination and subsequent degradation.

Identifier	Residue	Sequence	Organism
SIGNOR-145190	Ser196	RSLEVWGsQEALEEA	Homo sapiens
pmid	sentence
16540648	Atr was the major kinase responsible for the cellular phosphorylation of xpa following uv irradiation / we propose that the phosphorylation of xpa by atr checkpoint may positively regulate ner activity and thus may facilitate the cells to recover from ner-related dna damages.

Publications:

2

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-262666	Ser225	PFRCEFDsQASAPRA	Homo sapiens
pmid	sentence
23438602	HXRCC3 S225 phosphorylation is mediated by ATR via an ATM-dependent signaling pathway. These data clearly indicate that ATR mediates the late activation of XRCC3 following DSB accumulation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277296	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	Cell Line
SIGNOR-109420	Ser31	ALRLLDSsQIVIISA	Mus musculus	Thymocyte
pmid	sentence
11459832	These results thus suggest that this serine 31 residue is indeed an atm/atr phosphorylation site and in fact is the major site for atm/atr-mediated phosphorylation within e2f1. Thus, it is possible that the atm/atr-mediated phosphorylation inhibits the binding and function of skp2 and thus prevents the normal degradation of e2f1

Publications:

1

Organism:

Mus Musculus

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-134712	Ser317	ENVKYSSsQPEPRTG	Homo sapiens
pmid	sentence
15775976	Atr activation typically leads to chk1 phosphorylation and activation. In response to genotoxic stress, chk1 is phosphorylated on serines 317 (s317) and 345 (s345) by the ataxia-telangiectasia-related (atr) protein kinase.

Identifier	Residue	Sequence	Organism
SIGNOR-134716	Ser345	LVQGISFsQPTCPDH	Homo sapiens
pmid	sentence
15775976	Atr activation typically leads to chk1 phosphorylation and activation. In response to genotoxic stress, chk1 is phosphorylated on serines 317 (s317) and 345 (s345) by the ataxia-telangiectasia-related (atr) protein kinase.

Publications:

2

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-188666	Ser33	GFGSPAPsQAEKKSR	Homo sapiens
pmid	sentence
19843584	Atr phosphorylates s33 in response to replication stress

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-155214	Ser343	TTPGPSLsQGVSVDE	Homo sapiens
pmid	sentence
17526493	We demonstrate that mrn and atr/atr-interacting protein (trip) interact with each other, and the forkhead-associated/breast cancer c-terminal domains (fha/brct) of nbs1 play a significant role in mediating this interaction. Mutations in the fha/brct domains do not prevent atr activation but specifically impair atr-mediated nbs1 phosphorylation at ser-343, which results in a defect in the s-phase checkpoint.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-119546	Ser407	SSSIIYSsQEDVKEF	Homo sapiens	NCI-H1299 Cell
pmid	sentence
14654783	We found that a major kinase responsible for s407 phosphorylation is atrs407 phosphorylation of mdm2 by atr reduces mdm2-dependent export of p53 from nuclei to cytoplasm.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-177805	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-177809	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-177813	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-25151	Ser516	VHPPLPIsQSPENES	Homo sapiens
pmid	sentence
4709074	Mll is phosphorylated at serine 516 by atr in response to genotoxic stress in the s phase, which disrupts its interaction with, and hence its degradation by, the scf(skp2) e3 ligase, leading to its accumulation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-171290	Ser601	EMDLAHNsQSMHASS	Homo sapiens
pmid	sentence
21242293	Atr-mediated phosphorylation of dna polymerase _ is needed for efficient recovery from uv damage. We show that, after uv irradiation, pol_ becomes phosphorylated at ser601 by the ataxia-telangiectasia mutated and rad3-related (atr) kinase. Atr-dependent phosphorylation of pol_ is necessary to restore normal survival and postreplication repair

Publications:

1

Organism:

Homo Sapiens

Pathways:

DNA repair in cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-111248	Ser646	ETWSLPLsQNSASEL	Homo sapiens	HeLa Cell
pmid	sentence
11687627	Here we demonstrate that atr but not atm phosphorylates the human rad17 (hrad17) checkpoint protein on ser(635) and ser(645) in vitro.The rfc-related checkpoint protein rad17, a phosphorylation substrate of atr, is critical for atr-mediated checkpoint signaling and cell survival.

Identifier	Residue	Sequence	Organism
SIGNOR-111252	Ser656	SASELPAsQPQPFSA	Homo sapiens
pmid	sentence
11687627	Here we demonstrate that atr but not atm phosphorylates the human rad17 (hrad17) checkpoint protein on ser(635) and ser(645) in vitro.The rfc-related checkpoint protein rad17, a phosphorylation substrate of atr, is critical for atr-mediated checkpoint signaling and cell survival.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273516	Ser652	RLKSDVLsQLPAKQR	Homo sapiens	HEK-293 Cell
pmid	sentence
23873943	ATR phosphorylates SMARCAL1 on S652, thereby limiting its fork regression activities and preventing aberrant fork processing. Thus, phosphorylation of SMARCAL1 is one mechanism by which ATR prevents fork collapse, promotes the completion of DNA replication, and maintains genome integrity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275850	Ser67	DERVKEPsQDTVATE
pmid	sentence
31938050	Here we report that the deubiquitylase USP28 is recruited to sites of DNA damage in cisplatin-treated cells. ATR phosphorylates USP28 and increases its enzymatic activity.\|Representative immunoblots of n = 3. C Immunoblotting of total and phosphorylated USP28 at serine 67 and 714 in A431 cells exposed to indicated concentrations of CPPD for 6 h.

Identifier	Residue	Sequence
SIGNOR-275851	Ser714	ESSTNSSsQDYSTSQ
pmid	sentence
31938050	Here we report that the deubiquitylase USP28 is recruited to sites of DNA damage in cisplatin-treated cells. ATR phosphorylates USP28 and increases its enzymatic activity.\|Representative immunoblots of n = 3. C Immunoblotting of total and phosphorylated USP28 at serine 67 and 714 in A431 cells exposed to indicated concentrations of CPPD for 6 h.

Publications:

2

Identifier	Residue	Sequence	Organism
SIGNOR-129469	Ser68	EELDTLAsQALSQCP	Homo sapiens
pmid	sentence
15451423	When dna is damaged, the atr-atrip complex is recruited to chromatin and is activated to transduce the checkpoint signal, but the precise kinase activation mechanism remains unknown. Here, we show that atrip is phosphorylated in an atr-dependent manner after genotoxic stimuli. The serine 68 and 72 residues are important for the phosphorylation in vivo and are required exclusively for direct modification by atr in vitro.

Identifier	Residue	Sequence	Organism
SIGNOR-129473	Ser72	TLASQALsQCPAAAR	Homo sapiens
pmid	sentence
15451423	When dna is damaged, the atr-atrip complex is recruited to chromatin and is activated to transduce the checkpoint signal, but the precise kinase activation mechanism remains unknown. Here, we show that atrip is phosphorylated in an atr-dependent manner after genotoxic stimuli. The serine 68 and 72 residues are important for the phosphorylation in vivo and are required exclusively for direct modification by atr in vitro.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-149305	Ser717	KDGGPVTsQESGQKL	Homo sapiens
pmid	sentence
16943440	In the present study, we identify two novel dna damage-inducible phosphorylation sites on fancd2, threonine 691 and serine 717. Atr phosphorylates fancd2 on these two sites, thereby promoting fancd2 monoubiquitination and enhancing cellular resistance to dna cross-linking agents

Identifier	Residue	Sequence	Organism
SIGNOR-149309	Thr691	YGLEEYDtQDGIAIN	Homo sapiens
pmid	sentence
16943440	In the present study, we identify two novel dna damage-inducible phosphorylation sites on fancd2, threonine 691 and serine 717. Atr phosphorylates fancd2 on these two sites, thereby promoting fancd2 monoubiquitination and enhancing cellular resistance to dna cross-linking agents

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273517	Ser8	MEGPGLGsQCRNHSH	Mus musculus	Melanocyte
pmid	sentence
28869973	Collectively these results suggest that ZDHHC13 phosphorylation by ATR following UVB irradiation promotes its interaction with MC1R to stimulate MC1R palmitoylation.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-148722	Thr2609	LTPMFVEtQASQGTL	Homo sapiens
pmid	sentence
16908529	Finally, in vitro atr-mediated phosphorylation at the t2609 cluster was further confirmed by western blot analysis using phosphospecific antibodies against t2647 (fig. ?(Fig.7e),7e), suggesting that dna-pkcs could be the direct target of atr kinase.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism
SIGNOR-267662	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-81442	Thr68	SSLETVStQELYSIP	Homo sapiens	HEK-293 Cell
pmid	sentence
10973490	Atm- and rad3-related also phosphorylates thr68 in addition to thr26 and ser50, which are not phosphorylated to a significant extent by atm in vitro.Substitution of thr68 with ala reduced the extent of phosphorylation and activation of chk2 in response to ir

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	Cell Line
SIGNOR-262664	Thr826	KAAELTAtQVEEEEE	Homo sapiens	HCT-116 Cell
pmid	sentence
26082189	And-1 is phosphorylated at T826 by ATR following replication stress, and this phosphorylation is required for And-1 to accumulate at the damage sites, where And-1 promotes the interaction between Claspin and Chk1, thereby stimulating efficient Chk1 activation by ATR.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-200245	Thr859	WEVGFPStQTCMERG	Homo sapiens
pmid	sentence
23273981	Characterization of this site using phospho-specific antibodies and mutational analysis reveals that it is phosphorylated by atr and is required for binding of ctip to chromatin and subsequent processive resection.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-167632	Tyr291	DTDQLKLyEEPLSKL	Homo sapiens
pmid	sentence
20798688	C-abl can phosphorylate atr on y291 and y310 and this phosphorylation appears to have a positive role in atr activation under genotoxic stress.

Identifier	Residue	Sequence	Organism
SIGNOR-167636	Tyr310	FPFEAEAyRNIEPVY	Homo sapiens
pmid	sentence
20798688	C-abl can phosphorylate atr on y291 and y310 and this phosphorylation appears to have a positive role in atr activation under genotoxic stress.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Organism	Cell Line
SIGNOR-263232		Homo sapiens	U2-OS Cell
pmid	sentence
16530042	These results establish that TopBP1 can activate both Xenopus and human ATR. Furthermore, these experiments provide conclusive evidence that the kinase activity that is induced by TopBP1 is intrinsic to the ATR protein itself and is not due to a kinase that associates with ATR.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-169412		Homo sapiens
pmid	sentence
21070963	Together these data strongly support the conclusion that mec1 directly targets the s/tq sites in mcm4 and mcm6, although it is formally possible that mec1 and mrc1 activate a different s/tq-directed kinase to target mcm4 and mcm6.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-275841
pmid	sentence
28426283	It was reported that NEK1 associates with ATR/ATRIP and primes it for activation in response to a variety of genotoxic agents

Publications:

1

Identifier	Residue	Organism	Cell Line
SIGNOR-272822		Homo sapiens	HEK-293 Cell
pmid	sentence
25355518	USP20 phosphorylation by ATR is important for its stabilization and checkpoint activation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-201112		Homo sapiens
pmid	sentence
23422745	Atrand atm physically interacted with xpc and promptly localized to the uv damage sites.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-169450		Homo sapiens
pmid	sentence
21070963	Together these data strongly support the conclusion that mec1 directly targets the s/tq sites in mcm4 and mcm6, although it is formally possible that mec1 and mrc1 activate a different s/tq-directed kinase to target mcm4 and mcm6.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-263231		Homo sapiens	U2-OS Cell
pmid	sentence
16530042	These results establish that TopBP1 can activate both Xenopus and human ATR. Furthermore, these experiments provide conclusive evidence that the kinase activity that is induced by TopBP1 is intrinsic to the ATR protein itself and is not due to a kinase that associates with ATR.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-159933		Homo sapiens
pmid	sentence
18082599	Plk1 itself is negatively regulated by the ddr in an atm/atr-dependent manner.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-134781		Homo sapiens
pmid	sentence
15775976	Regulation of NF-kappaB and p53 through activation of ATR and Chk1 by the ARF tumour suppressorInduction of ATR activity in Hs68 E2F1ER cells by endogenous ARF.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Organism	Cell Line
SIGNOR-173966		Homo sapiens	HEK-293 Cell
pmid	sentence
21615992	Binding of myh directly participates in atr and topbp1 activation in dna damage signaling, leading to apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-201050		Homo sapiens
pmid	sentence
23422745	The phosphorylation of atr and atm substrates, chk1, chk2, h2ax, and brca1 was significantly reduced or abrogated in mutant cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Organism
SIGNOR-242609		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:

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-130187		Homo sapiens
pmid	sentence
15530773	The pikk kinases serve as transducers of the damege signel, ultimately phosphorylating and activating the downstream effector kinases: checkpoint kinases 1 and 2.

Publications:

1

Organism:

Homo Sapiens

Name	ATR View Modifications
Full Name	Serine/threonine-protein kinase ATR
Synonyms	Ataxia telangiectasia and Rad3-related protein, FRAP-related protein 1 \| FRP1
Primary ID	Q13535
Links	- -
Type	protein
Relations	63
Pathways	DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer
Function	Serine/threonine protein kinase which activates checkpoint signaling upon genotoxic stresses such as ionizing radiation (IR), ultraviolet light (UV), or DNA replication stalling, thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates BRCA1, CHEK1, MCM2, RAD17, RPA2, SMC1 and p53/TP53, which collectively inhibit DNA replication and mitosis and promote DNA repair, recombination and apoptosis. Phosphorylates 'Ser-139' of histone variant H2AX at sites of DNA damage, thereby regulating DNA damage response mechanism. Required for FANCD2 ubiquitination. Critical for maintenance of fragile site stability and efficient regulation of centrosome duplication. Positively regulates the restart of stalled replication forks following activation by the KHDC3L-OOEP scaffold complex (By similarity).

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