HCSGD entry for CHEK2


1. General information

Official gene symbolCHEK2
Entrez ID11200
Gene full namecheckpoint kinase 2
Other gene symbolsCDS1 CHK2 HuCds1 LFS2 PP1425 RAD53 hCds1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000077DNA damage checkpointIEA TASbiological_process
GO:0000086G2/M transition of mitotic cell cycleIMPbiological_process
GO:0000781Chromosome, telomeric regionIDAcellular_component
GO:0004672Protein kinase activityIEAmolecular_function
GO:0004674Protein serine/threonine kinase activityIDA IEA TASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005524ATP bindingIEAmolecular_function
GO:0005654NucleoplasmTAScellular_component
GO:0006302Double-strand break repairIMPbiological_process
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0006355Regulation of transcription, DNA-templatedIDAbiological_process
GO:0006468Protein phosphorylationIDAbiological_process
GO:0006915Apoptotic processIEAbiological_process
GO:0006974Cellular response to DNA damage stimulusIMP TASbiological_process
GO:0006975DNA damage induced protein phosphorylationIMPbiological_process
GO:0008630Intrinsic apoptotic signaling pathway in response to DNA damageIDA IMPbiological_process
GO:0010332Response to gamma radiationIEAbiological_process
GO:0016605PML bodyIDAcellular_component
GO:0019901Protein kinase bindingIPImolecular_function
GO:0031625Ubiquitin protein ligase bindingIPImolecular_function
GO:0042176Regulation of protein catabolic processIMPbiological_process
GO:0042770Signal transduction in response to DNA damageIDA IEAbiological_process
GO:0042802Identical protein bindingIPImolecular_function
GO:0042803Protein homodimerization activityIDAmolecular_function
GO:0044257Cellular protein catabolic processIMPbiological_process
GO:0045893Positive regulation of transcription, DNA-templatedIDAbiological_process
GO:0046777Protein autophosphorylationIDAbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0050821Protein stabilizationIDAbiological_process
GO:0072428Signal transduction involved in intra-S DNA damage checkpointIMPbiological_process
GO:0090307Spindle assembly involved in mitosisIMPbiological_process
GO:0090399Replicative senescenceNASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.58348763720.04555682150.99999024730.4005978993

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up0.2520227624
GSE13712_SHEARDown-0.1198285260
GSE13712_STATICDown-0.5030174769
GSE19018Up0.1128408565
GSE19899_A1Up0.0157198515
GSE19899_A2Down-0.2199920518
PubMed_21979375_A1Up0.3937713341
PubMed_21979375_A2Up0.1788714257
GSE35957Down-1.1493536117
GSE36640Down-0.3312557853
GSE54402Down-0.5912164416
GSE9593Down-0.3496203060
GSE43922Up0.0564406893
GSE24585Down-0.3218441818
GSE37065Up0.0952316041
GSE28863_A1Down-0.6960496006
GSE28863_A2Down-0.4580706578
GSE28863_A3Up0.0666491934
GSE28863_A4Up0.4777863982
GSE48662Down-0.0389491289

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

XL844DB05149 -

  • MicroRNAs

    • mirTarBase
No target information from mirTarBase
    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 23 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26690546Under such conditions, Chk2, cyclin A/CDK2 and ERK1/2 were aberrantly activated
26690546Pharmacological inactivation of Chk2, CDK2 or ERK1/2 or depletion of CDK2 or Chk2 inhibited the centrosome amplification in ETO-treated ACT cells
26690546Chloroquine alleviated CDK2 and ERK, but not Chk2, activation and thus inhibited centrosome amplification in either ETO- or hydroxyurea-treated ACT cells
25801233After irradiation, the p21 protein was increased and Chk1 and Chk2 were activated
25744025However, ATM signalling and DNA repair remained intact after lamins A/C depletion, whereas nesprin-2 disruption ablated downstream Chk2 activation and induced genomic instability
23253087Two separate defects in p53 signaling appeared common: in nevi, lack of p53 phosphorylation by activated CHEK2, and in melanomas, defective p21 upregulation by p53 even when phosphorylated
23229510E235 also activated DNA damage response signaling, resulting in increased levels of Ser15-phosphorylated p53, gamma-H2AX, and phosphorylated checkpoint kinase 2 (Chk2), although E235 does not appear to cause physical DNA damage
22952233Notably, these cells had increased levels of spontaneous DNA damage and phosphorylated CHK2
22417805We assessed the effect of garcinol on the cell cycle checkpoint after IR treatment by analyzing the phosphorylation levels of checkpoint kinases CHK1 and CHK2 and histone H3, and by cell cycle profile analysis using flow cytometry
21671044Crucial components in the cascade of DNA damage response, including ataxia telangiectasia mutated, CHK2, p53, p21 and p16/p19(ARF), play important roles in HSC maintenance and self-renewal in the scenarios of both sufficient telomere reserve and dysfunctional telomere
21149450The TopBP1-ablated mouse cells exhibit phosphorylation of H2AX and Chk2, indicating that the cells contain DNA breaks
21118958Unlike transient foci, DNA-SCARS associate with PML nuclear bodies, lack the DNA repair proteins RPA and RAD51, lack single-stranded DNA and DNA synthesis and accumulate activated forms of the DDR mediators CHK2 and p53
21118958Importantly, depletion of the DNA-SCARS-stabilizing component histone H2AX did not deplete 53BP1 from DNA-SCARS but diminished the presence of MDC1 and activated CHK2
20947452Here we show pronounced senescence in pol mu(-)(/)(-) MEFs, associated with high levels of the tumor-suppressor p16(INK4A) and the DNA damage response kinase CHK2
20647331As the passage number increased, markers of DNA damage, including the level of gammaH2AX and CHK2 phosphorylation, were seen
20457353Radiation-induced gamma-H2AX and Chk2 phosphorylation were induced transiently in securin-wild-type cells but exhibited sustained activation in securin-null cells
20089117Overexpression of the mutant protein in primary fibroblasts is associated with telomere-based cellular senescence, multinucleated cells and the activation of the DNA damage response genes ATM, Chk2 and p53
20042274Inhibition of ATM in A2780 cells, resulting in reduced phosphorylation of Chk2, enhanced ST1968-induced apoptosis, but had no effect in KB cells
19906512RESULTS: We now report that T-oligo increases the level of the antioxidant enzymes superoxide dismutase 1 and 2 and protects cells from oxidative damage; and that telomere-based gammaH2AX (DNA damage) foci that form in response to T-oligos contain phosphorylated ATM and Chk2, proteins known to activate p53 and to mediate cell cycle arrest in response to oxidative stress
18440596The cellular DNA damage response (DDR) entails the activation of ATM, ATR and/or DNA PK protein kinases that causes modifications of proteins including Chk1, Chk2 and 53BP1, aggregation of DDR proteins into foci, and activation of p53
16317088The Chk2 kinase is a tumor suppressor and key component of the DNA damage checkpoint response that encompasses cell cycle arrest, apoptosis, and DNA repair
16317088High-level expression of virally transduced Chk2 in A549 human lung carcinoma cells led to arrested proliferation, apoptosis, and senescence
16317088Small interfering RNA-mediated knockdown of p21 in p53-defective cells expressing Chk2 resulted in a decrease in senescent cells
16317088These results revealed a p53-independent role for Chk2 in p21 induction and senescence that may contribute to tumor suppression and genotoxic treatment outcome
15930307These results show that whereas Akt activation suppresses temozolomide-induced Chk2 activation and G2 arrest, the overriding effect is protection from temozolomide-induced cytotoxicity
15760303After DNA damage, activation of Rad53, which together with Chk1 represents a protein kinase central to all checkpoint pathways, normally requires Rad9, a checkpoint adaptor
15760303RESULTS: We report that in telomerase-negative (tlc1Delta) cells, activation of Rad53, although diminished, could still take place in the absence of Rad9
15760303In contrast, Rad9 was essential for Rad53 activation in cells that entered senescence in the presence of functional telomerase, namely in senescent cells bearing mutations in telomere end-protection proteins (cdc13-1 yku70Delta)
15760303In telomerase-negative cells deleted for RAD9, Mrc1, another checkpoint adaptor previously implicated in the DNA replication checkpoint, mediated Rad53 activation
15760303Rad9 and Rad53, as well as other DNA damage checkpoint proteins (Mec1, Mec3, Chk1 and Dun1), were required for complete DNA-damage-induced cell-cycle arrest after loss of telomerase function
15610769X facilitates the formation of DNA damage foci around uncapped telomeres, and this in turn activates downstream kinases Chk1 and Chk2 and, eventually, p53
15467458Dysfunctional telomeres at senescence signal cell cycle arrest via Chk2
15467458We have recently linked the phosphorylation and activation of one major DNA damage effector checkpoint kinase, Chk2, to telomere erosion in signalling cell cycle arrest in normal fibroblasts
14608368We also show that senescent cells contain activated forms of the DNA damage checkpoint kinases CHK1 and CHK2
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