Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-278161	Ser100	VSYARPSsEVIKDAN	Homo sapiens
pmid	sentence
21745814	Taken together, these findings indicate that phosphorylation at residue S100 by Chk2 enhances HuR-binding to the occludin mRNA, while phosphorylation at S88 and T118 reduces this interaction; these modifications in turn regulate occludin translation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-177091	Ser111	GTGRRIHsYRGHLWL	Homo sapiens	Kidney Cancer Cell
pmid	sentence
22071692	We demonstrated that checkpoint kinase-2 (chk2) binds to the beta-domain of pvhl and phosphorylates ser 111 on dna damage. Notably, this modification enhances pvhl-mediated transactivation of p53 by recruiting p300 and tip60 to the chromatin of p53 target gene

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-94872	Ser117	ESLQRRLsVYRQIVD	Homo sapiens
pmid	sentence
12402044	Hcds1/chk2 phosphorylates pml at ser 117 in vitro. hcds1/chk2 phosphorylates pml in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-99721	Ser124	PALKRSHsDSLDHDI	Homo sapiens
pmid	sentence
12676583	We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases.

Identifier	Residue	Sequence	Organism
SIGNOR-260778	Ser124	PALKRSHsDSLDHDI	Homo sapiens
pmid	sentence
11298456	We conclude that Chk2-dependent phosphorylation of Cdc25A on Serâ€‰123 represents a critical step in promoting its rapid destruction in response to IR-induced DNA damage.

Identifier	Residue	Sequence	Organism
SIGNOR-106808	Ser124	PALKRSHsDSLDHDI	Homo sapiens
pmid	sentence
11298456	We show that IR-induced destruction of Cdc25A requires both ATM and the Chk2-mediated phosphorylation of Cdc25A on serine 123.

Identifier	Residue	Sequence	Organism
SIGNOR-118759	Ser178	LFTQRQNsAPARMLS	Homo sapiens
pmid	sentence
14559997	The order and fidelity of cell cycle events in mammals is intimately linked to the integrity of the Chk1 kinase-Cdc25A phosphatase pathway. Chk1 phosphorylation targets Cdc25A for destruction and, as shown here, inhibits interactions between Cdc25A and its mitotic substrate cyclin B1-Cdk1. Phosphorylation of Cdc25A on serine 178 and threonine 507 facilitates 14-3-3 binding, and Chk1 phosphorylates both residues in vitro.

Identifier	Residue	Sequence	Organism
SIGNOR-99725	Ser178	LFTQRQNsAPARMLS	Homo sapiens
pmid	sentence
12676583	We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases.

Identifier	Residue	Sequence	Organism
SIGNOR-99729	Ser279	VLKRPERsQEESPPG	Homo sapiens
pmid	sentence
12676583	We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases.

Identifier	Residue	Sequence	Organism
SIGNOR-99733	Ser293	GSTKRRKsMSGASPK	Homo sapiens
pmid	sentence
12676583	We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases.

Publications:

7

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-260835	Ser124	PALKRSHsDSLDHDI	Homo sapiens
pmid	sentence
12676583	Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A \| Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A

Identifier	Residue	Sequence	Organism
SIGNOR-260833	Ser178	LFTQRQNsAPARMLS	Homo sapiens
pmid	sentence
12676583	Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A \| Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A

Identifier	Residue	Sequence	Organism
SIGNOR-260834	Ser279	VLKRPERsQEESPPG	Homo sapiens
pmid	sentence
12676583	Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A \| Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A

Identifier	Residue	Sequence	Organism
SIGNOR-260836	Ser293	GSTKRRKsMSGASPK	Homo sapiens
pmid	sentence
12676583	Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A \| Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A

Publications:

4

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264416	Ser143	SKKSRSHsAKTPGFS	Homo sapiens	HCT-116 Cell
pmid	sentence
17157788	Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.\| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264417	Ser477	ELIERKTsSLDPNDQ	Homo sapiens	HCT-116 Cell
pmid	sentence
17157788	Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.\| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264418	Ser510	KKVDRKAsKGRKLRF	Homo sapiens	HCT-116 Cell
pmid	sentence
17157788	Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.\| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-75629	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
10710310	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-75009	Ser15	PSVEPPLsQETFSDL	Homo sapiens	HeLa Cell
pmid	sentence
10673501	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-153463	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
17339337	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability. We have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-74823	Ser15	PSVEPPLsQETFSDL	Homo sapiens
pmid	sentence
10656682	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-77144	Ser20	PLSQETFsDLWKLLP	Homo sapiens
pmid	sentence
10801407	The tumour suppressor protein p53 is stabilised and activated in response to ionising radiation. This is known to depend on the kinase atm;recent results suggest atm acts via the downstream kinase chk2/hcds1, which stabilises p53 at least in part by direct phosphorylation of residue serine 20

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-75633	Ser366	PGGSRAHsSHLKSKK	Homo sapiens	LNCaP Cell
pmid	sentence
15659650	The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-75013	Ser366	PGGSRAHsSHLKSKK	Homo sapiens	HeLa Cell
pmid	sentence
10673501	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-75017	Ser37	NVLSPLPsQAMDDLM	Homo sapiens	HeLa Cell
pmid	sentence
10673501	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-153475	Ser37	NVLSPLPsQAMDDLM	Homo sapiens
pmid	sentence
15659650	The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. On activation, both of these kinases also phosphorylate multiple sites in the p53 N-terminal domain. These include Ser15, Thr18, Ser20, and Ser37, which are all DNA-damageinducible sites

Identifier	Residue	Sequence	Organism
SIGNOR-75637	Ser37	NVLSPLPsQAMDDLM	Homo sapiens
pmid	sentence
10710310	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-74831	Ser37	NVLSPLPsQAMDDLM	Homo sapiens
pmid	sentence
10656682	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-74835	Ser378	SKKGQSTsRHKKLMF	Homo sapiens	LNCaP Cell
pmid	sentence
15659650	The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage.

Identifier	Residue	Sequence	Organism
SIGNOR-75641	Ser378	SKKGQSTsRHKKLMF	Homo sapiens
pmid	sentence
10710310	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-153479	Ser378	SKKGQSTsRHKKLMF	Homo sapiens	B-lymphocyte
pmid	sentence
17339337	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-74839	Thr18	EPPLSQEtFSDLWKL	Homo sapiens
pmid	sentence
10656682	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism
SIGNOR-75645	Thr18	EPPLSQEtFSDLWKL	Homo sapiens
pmid	sentence
10710310	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-153483	Thr18	EPPLSQEtFSDLWKL	Homo sapiens	B-lymphocyte
pmid	sentence
17339337	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-75025	Thr18	EPPLSQEtFSDLWKL	Homo sapiens	HeLa Cell
pmid	sentence
10673501	Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53.

Publications:

18

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-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
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.

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.

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-260776	Ser20	PLSQETFsDLWKLLP	Homo sapiens
pmid	sentence
17339337	Evaluation of these calcium calmodulin kinase superfamily members as candidate Ser(20) kinases in vivo has shown that only CHK1 or DAPK-1 can stimulate p53 transactivation and induce Ser(20) phosphorylation of p53.\| Thus, endogenous CHK1 is required for the majority of Ser20 site phosphorylation of ectopically expressed p53 in H1299 cells.

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-102779	Ser216	SGLYRSPsMPENLNR	Homo sapiens
pmid	sentence
12835754	Activated chk2 in turn phosphorylates cdc25c at serine-216 contributing to the g2/m checkpoints. Cds1 phosphorylates and inactivates cdc25 in vitro\|CDC25C is phosphorylated on Ser 216 throughout interphase, but not in mitosis. This creates a binding site for 14‐3‐3 proteins \| It has been suggested that 14‐3‐3 protein binding is responsible for retaining Cdc25C in the cytoplasm during interphase, thereby contributing to the prevention of premature initiation of mitotic events

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273611	Ser247	EKIKRPRsSNAETLY	Homo sapiens	U2-OS Cell
pmid	sentence
25361978	REGγ interacts with DBC1 and is phosphorylated by Chk2.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-150843	Ser287	PITHDDVsSIFLNSE	Homo sapiens
pmid	sentence
17110335	During interphase, cdc25 is inhibited by ser287 phosphorylation (xenopus cdc25;ser 216 in human cdc25c) and this inhibitory phosphorylation is maintained by dna-responsive checkpoints / s287 is targeted by many kinases, including chk1, chk2, ctak-1, pka, p38 and mapkap kinase-2 suggesting that phosphorylation of this site may integrate multiple signaling inputs.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-140417	Ser342	SKLTHSLsTSDITAI	Homo sapiens
pmid	sentence
16163388	Phosphorylation of s342 and s367 in vivo require the chk2 kinase. Chk2 also stimulates mdmx ubiquitination and degradation by mdm2

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-260822	Ser364	PLLSRMGsLRAPVDE	Homo sapiens
pmid	sentence
12717439	Therefore, Chk2 phosphorylates and activates E2F-1 in response to DNA damage, resulting in apoptosis. \| These results suggest that the Ser 364 site is phosphorylated by Chk2 and that anti-P-Ser 364 recognises the phosphorylated site in E2F-1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-197278	Ser364	PLLSRMGsLRAPVDE	Homo sapiens
pmid	sentence
22558186	Among these effector proteins, chk1 phosphorylates tlk12 and rad51, while brca, pik3, pml and e2f1 are chk2 substrates.

Identifier	Residue	Sequence	Organism
SIGNOR-100898	Ser364	PLLSRMGsLRAPVDE	Homo sapiens
pmid	sentence
12717439	We report that checkpoint kinase 2 (chk2) regulates e2f-1 activity in response to the dna-damaging agent etoposide. A chk2 consensus phosphorylation site in e2f-1 is phosphorylated in response to dna damage

Publications:

2

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism
SIGNOR-178071	Ser367	PDCRRTIsAPVVRPK	Homo sapiens
pmid	sentence
18356162	The chk1 and chk2 kinases have also been shown to phosphorylate ser367, leading to 14-3-3 binding (34_36, 38, 44). In both cases, the outcome differed: in chk1-mediated phosphorylation, mdmx was translocated to the cytoplasm;in chk2-mediated phosphorylation, mdmx was degraded (34_36, 38, 44). It is possible that the damage response is mediated through additional phosphorylation sites other than ser367 and that, depending on the type of damage, certain sites will be modified, leading to different outcomes.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-150746	Ser376	PLLPRVSsYLVPIQF	Homo sapiens	U2-OS Cell
pmid	sentence
17101782	Chk2 mediates stabilization of the foxm1 transcription factor to stimulate expression of dna repair genesthis phosphorylation of foxm1 on serine residue 361 caused increased stability of the foxm1 protein

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-179537	Ser379	SKILGETsLMRTLCG	Homo sapiens	HEK-293 Cell
pmid	sentence
18644861	Regulation of chk2 ubiquitination and signaling through autophosphorylation of serine 379.Thus, auto-/transphosphorylation of s379 is required for chk2 ubiquitination and effector function

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-103544	Ser516	PQVLAQPsTSRKRPR	Homo sapiens	HCT-15 Cell
pmid	sentence
12855706	Chk2 is also autophosphorylated following dna damage. It is proposed that autophosphorylation of chk2 may contribute to chk2 activation. To fully understand the regulation of chk2, we mapped an in vitro chk2 autophosphorylation site at c-terminal serine 516 site (ser-516). Ser-516 of chk2 is phosphorylated following radiation in vivo, and this phosphorylation depends on the kinase activity of chk2.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-116127	Thr383	GETSLMRtLCGTPTY	Homo sapiens	HEK-293 Cell
pmid	sentence
11901158	Phosphorylation of thr-68 by the ataxia telangiectasia-mutated is necessary for efficient activation of chk2 when cells are exposed to ionizing radiation. By an unknown mechanism, this initial event promotes additional autophosphorylation events including modifications of thr-383 and thr-387

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-116131	Thr387	LMRTLCGtPTYLAPE	Homo sapiens	HEK-293 Cell
pmid	sentence
11901158	Phosphorylation of thr-68 by the ataxia telangiectasia-mutated is necessary for efficient activation of chk2 when cells are exposed to ionizing radiation. By an unknown mechanism, this initial event promotes additional autophosphorylation events including modifications of thr-383 and thr-387

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-116135	Thr68	SSLETVStQELYSIP	Homo sapiens	HEK-293 Cell
pmid	sentence
11901158	Thus, activation of chk2 in irradiated cells may occur through oligomerization of chk2 via binding of the thr-68-phosphorylated region of one chk2 to the fha domain of another. Oligomerization of chk2 may therefore increase the efficiency of trans-autophosphorylation resulting in the release of active chk2 monomers that proceed to enforce checkpoint control in irradiated cells.

Publications:

5

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-277790	Ser55	LEKLLASsINGVRCP	Homo sapiens	HEK-293 Cell
pmid	sentence
37943659	We show that CHK2 binds and phosphorylates TRIM32 at the S55 site, which then mediates K63-linked ubiquitination of ATG7 at the K45 site to initiate autophagy.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277804	Ser55	LEKLLASsINGVRCP	Homo sapiens	HEK-293 Cell
pmid	sentence
37943659	We show that CHK2 binds and phosphorylates TRIM32 at the S55 site, which then mediates K63-linked ubiquitination of ATG7 at the K45 site to initiate autophagy.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-171026	Ser579	NVKSKIGsTENLKHQ	Homo sapiens
pmid	sentence
21215781	Tau pseudophosphorylation at specific sites such as s262, s293, s324 and s356 was reported to induce tau conformational change and attenuate tau binding to microtubules (fischer et al., 2009). Then, newly soluble tau proteins are targeted by post-translational modifications that directly or indirectly alter tau conformation, promoting tau dimerization in an anti-parallel manner. Stable tau dimers form tau oligomers, which continue in the aggregation process

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-262794	Ser60	DNTAGCTsAGPHFNP	Saccharomyces cerevisiae
pmid	sentence
24647101	ROS signaling is mediated by Mec1/ATM and its effector Dun1/Cds1 kinase, through Dun1 interaction with Sod1 and regulation of Sod1 by phosphorylation at S60, 99. In the nucleus, Sod1 binds to the promoters and regulates the expression of oxidative resistance and repair genes.

Identifier	Residue	Sequence	Organism
SIGNOR-262795	Ser99	KDGVADVsIEDSVIS	Saccharomyces cerevisiae
pmid	sentence
24647101	ROS signaling is mediated by Mec1/ATM and its effector Dun1/Cds1 kinase, through Dun1 interaction with Sod1 and regulation of Sod1 by phosphorylation at S60, 99. In the nucleus, Sod1 binds to the promoters and regulates the expression of oxidative resistance and repair genes.

Publications:

2

Organism:

Saccharomyces Cerevisiae

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-153908	Ser612	MYLSPVRsPKKKGST	Homo sapiens	MCF-7 Cell
pmid	sentence
17380128	Phosphorylation of prb at ser612 by chk1/2 leads to a complex between prb and e2f-1 after dna damageprb inhibits cell cycle progression through interactions with the e2f family of transcription factors. Here, we report that dna damage induced not only the dephosphorylation of prb at cdk phosphorylation sites and the binding of prb to e2f-1, but also the phosphorylation of prb at ser612. Phosphorylation of prb at ser612 enhanced the formation of a complex between prb and e2f-1

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-276052	Ser62	SSSGTLSsLETVSTQ	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.

Identifier	Residue	Sequence	Organism
SIGNOR-276051	Ser73	VSTQELYsIPEDQEP	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:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-278163	Ser88	LNGLRLQsKTIKVSY	Homo sapiens
pmid	sentence
21745814	Given the fact that Chk2 phosphorylates HuR at residues S88, S100 and T118 and that each individual phosphorylation site by Chk2 plays a distinct role in regulating HuR- binding to different target mRNAs (22,42), we further tested HuR mutants with alanine substitutions at each of the Chk2 phosphorylation sites.

Identifier	Residue	Sequence	Organism
SIGNOR-278162	Thr118	SGLPRTMtQKDVEDM	Homo sapiens
pmid	sentence
21745814	Given the fact that Chk2 phosphorylates HuR at residues S88, S100 and T118 and that each individual phosphorylation site by Chk2 plays a distinct role in regulating HuR- binding to different target mRNAs, we further tested HuR mutants with alanine substitutions at each of the Chk2 phosphorylation sites.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264557	Ser90	IPPARMMsTESANSF	Homo sapiens	NCI-H1299 Cell
pmid	sentence
32187724	We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in a ROS-dependent fashion.\|CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, promoting autophagy via Beclin 1 release from Bcl‐2 sequestration

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264556	Ser93	ARMMSTEsANSFTLI	Homo sapiens	NCI-H1299 Cell
pmid	sentence
32187724	We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in a ROS-dependent fashion.\|CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, promoting autophagy via Beclin 1 release from Bcl‐2 sequestration

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-120575	Ser988	PPLFPIKsFVKTKCK	Homo sapiens	Breast Cancer Cell
pmid	sentence
14701743	In this study, we tested the hypothesis that the brca1-mediated regulation of recombination requires the chk2- and atm-dependent phosphorylation sites.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276908	Thr182	SHFVRVStAQKSKKG	Homo sapiens	HEK-293T Cell
pmid	sentence
26028025	We now provide evidence that BLM undergoes K48-linked ubiquitylation and subsequent degradation during mitosis due to the E3 ligase, Fbw7α. Fbw7α carries out its function after GSK3β- and CDK2/cyclin A2-dependent phosphorylation events on Thr171 and Ser175 of BLM which lies within a well-defined phosphodegron, a sequence which is conserved in all primates.Phosphorylation on BLM Thr171 and Ser175 depends on prior phosphorylation at Thr182 by Chk1/Chk2. Thr182 phosphorylation not only controls BLM ubiquitylation and degradation during mitosis but is also a determinant for its localization on the ultrafine bridges.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-249180	Thr26	SQPHGSVtQSQGSSS	in vitro
pmid	sentence
12493754	Plk1 overexpression enhances phosphorylation of Chk2 at Thr-68. Plk1 phosphorylates recombinant Chk2 in vitro.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-181816	Thr284	APTRTPAtAPVPARA	Homo sapiens
pmid	sentence
18971944	Chk2 formed a complex with xrcc1, the ber scaffold protein, and phosphorylated xrcc1 in vivo and in vitro at thr(284). our results are consistent with the phosphorylation of xrcc1 by atm-chk2 facilitating recruitment of downstream ber proteins to the initial damage recognition/excision step to promote ber.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-183470	Thr288	SPDCDVKtDDSVVPC	Homo sapiens
pmid	sentence
19151762	Phosphorylation at ttk/hmps1 thr288 is enhanced by chk2 in vitro and in vivo after ir

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-242665	Thr288	SPDCDVKtDDSVVPC	Homo sapiens
pmid	sentence
19151762	Phosphorylation at ttk/hmps1 thr288 is enhanced by chk2 in vitro and in vivo after ir

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-248617	Thr68	SSLETVStQELYSIP	Homo sapiens	Ovary Cancer Cell
pmid	sentence
16596250	Protein phosphatase 2A interacts with Chk2 and regulates phosphorylation at Thr-68 after cisplatin treatment of human ovarian cancer cells\|In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-248582	Thr68	SSLETVStQELYSIP	Homo sapiens
pmid	sentence
16596250	Protein phosphatase 2A interacts with Chk2 and regulates phosphorylation at Thr-68 after cisplatin treatment of human ovarian cancer cells\|In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-96637	Thr68	SSLETVStQELYSIP	Homo sapiens
pmid	sentence
12493754	Plk1 overexpression enhances phosphorylation of chk2 at thr-68.

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
SIGNOR-133384	Thr68	SSLETVStQELYSIP	Homo sapiens
pmid	sentence
15668230	We have found that dna-pk is the major constituent of an activity present in extracts of mammalian cells that phosphorylates chk2. Our results suggest that hypophosphorylated chk2 can be phosphorylated at thr68 by dna-pk in vitro.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Cell cycle: G2/M phase transition

Identifier	Residue	Sequence	Organism
SIGNOR-132665	Thr68	SSLETVStQELYSIP	Homo sapiens
pmid	sentence
15618221	Ttk/hmps1 directly phosphorylates chk2 on thr-68 in vitro.ablation of ttk expression using small interfering rna results not only in reduced chk2 thr-68 phosphorylation, but also in impaired growth arrest. Our results are consistent with a model in which ttk functions upstream from chk2 in response to dna damage

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-248318	Thr68	SSLETVStQELYSIP	in vitro
pmid	sentence
16311512	an in vitro phosphatase assay revealed that Wip1 (WT), but not Wip1 (D314A), dephosphorylates Thr68 on phosphorylated Chk2 in vitro, resulting in the inhibition of Chk2 kinase activity toward glutathione S-transferase-Cdc25C.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-206841		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-190206		Homo sapiens
pmid	sentence
Other

Identifier	Residue	Organism
SIGNOR-163119		Homo sapiens
pmid	sentence
20068082	Azd7762 is equally potent against chk2 in vitro.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-267228		Homo sapiens	HCT-116 Cell
pmid	sentence
21351257	The human protein N(α)-terminal acetyltransferase A complex (hNatA), composed of the catalytic hNaa10p (hArd1) and auxiliary hNaa15p (hNat1/NATH/Tubedown) subunits, was reported to be important for cell survival and growth of various types of cancer. lack of acetylation by hNatA activated H2A.X and Chk2 in both HCT116 cell lines independent of TP53 status (Fig. 6).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-242605		Homo sapiens
pmid	sentence
19151762	Cell cycle progression is monitored constantly to ensure faithful passage of genetic codes and genome stability. We have demonstrated previously that, upon DNA damage, TTK/hMps1 activates the checkpoint kinase CHK2 by phosphorylating CHK2 at Thr68

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	Cell Line
SIGNOR-263262		Homo sapiens	HeLa Cell
pmid	sentence
23438602	Interestingly, as with ATM (40, 41), XRCC3-deficient cells exhibited RDS and impaired CHK2 activation\|Notably, early activation of CHK2 in S/G2 phase was downstream of XRCC3 recruitment as well as its phosphorylation at the sites of DSBs. NBS1 also has been shown to be involved in the early activation of CHK2 in response to IR (42). It is likely that NBS1-dependent CHK2 phosphorylation is mediated through XRCC3 activation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-263261		Homo sapiens	HeLa Cell
pmid	sentence
23438602	Interestingly, as with ATM (40, 41), XRCC3-deficient cells exhibited RDS and impaired CHK2 activation\|Notably, early activation of CHK2 in S/G2 phase was downstream of XRCC3 recruitment as well as its phosphorylation at the sites of DSBs. NBS1 also has been shown to be involved in the early activation of CHK2 in response to IR (42). It is likely that NBS1-dependent CHK2 phosphorylation is mediated through XRCC3 activation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-197281		Homo sapiens
pmid	sentence
22558186	In this report, we characterize the binding of sh2(chk) to specific phosphotyrosine sites on the c-kit protein sequence. the sh2(chk) binding to the two sites is direct and not through phosphorylated intermediates such as fyn or shc. this indicates that chk binds to the same site on c-kit to which fyn binds, possibly bringing the two into proximity on associated c-kit subunits and leading to the down-regulation of fyn by chk.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-163234		Homo sapiens
pmid	sentence
20068082	Xl844 (exelixis) a potent atp-competitive inhibitor of chk1 (ki, 2.2nm) and chk2 (ki, 0.07nm).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-129255		Homo sapiens	HEK-293 Cell
pmid	sentence
15380617	Found that chk2 associated with the b' regulatory subunit of protein phosphatase pp2a. In vitro kinase assays showed that b'gamma3 was a potent chk2 substrate. This phosphorylation increased the catalytic phosphatase activity of pp2a.

Publications:

1

Organism:

Homo Sapiens

Name	CHEK2 View Modifications
Full Name	Serine/threonine-protein kinase Chk2
Synonyms	CHK2 checkpoint homolog, Cds1 homolog, Hucds1, hCds1, Checkpoint kinase 2 \| CDS1, CHK2, RAD53
Primary ID	O96017
Links	- -
Type	protein
Relations	93
Pathways	DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer
Inhibitors	6-bromo-3-(1-methyl-4-pyrazolyl)-5-(3-piperidinyl)-7-pyrazolo[1,5-a]pyrimidinamine; 3-(carbamoylamino)-5-(3-fluorophenyl)-N-[(3S)-3-piperidinyl]-2-thiophenecarboxamide; SCHEMBL14517914
Function	Serine/threonine-protein kinase which is required for checkpoint-mediated cell cycle arrest, activation of DNA repair and apoptosis in response to the presence of DNA double-strand breaks. May also negatively regulate cell cycle progression during unperturbed cell cycles. Following activation, phosphorylates numerous effectors preferentially at the consensus sequence [L-X-R-X-X-S/T]. Regulates cell cycle checkpoint arrest through phosphorylation of CDC25A, CDC25B and CDC25C, inhibiting their activity. Inhibition of CDC25 phosphatase activity leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes and blocks cell cycle progression. May also phosphorylate NEK6 which is involved in G2/M cell cycle arrest. Regulates DNA repair through phosphorylation of BRCA2, enhancing the association of RAD51 with chromatin which promotes DNA repair by homologous recombination. Also stimulates the transcription of genes involved in DNA repair (including BRCA2) through the phosphorylation and activation of the transcription factor FOXM1. Regulates apoptosis through the phosphorylation of p53/TP53, MDM4 and PML. Phosphorylation of p53/TP53 at 'Ser-20' by CHEK2 may alleviate inhibition by MDM2, leading to accumulation of active p53/TP53. Phosphorylation of MDM4 may also reduce degradation of p53/TP53. Also controls the transcription of pro-apoptotic genes through phosphorylation of the transcription factor E2F1. Tumor suppressor, it may also have a DNA damage-independent function in mitotic spindle assembly by phosphorylating BRCA1. Its absence may be a cause of the chromosomal instability observed in some cancer cells. Promotes the CCAR2-SIRT1 association and is required for CCAR2-mediated SIRT1 inhibition (PubMed:25361978).

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