HCSGD entry for CHEK1
1. General information
| Official gene symbol | CHEK1 |
|---|---|
| Entrez ID | 1111 |
| Gene full name | checkpoint kinase 1 |
| Other gene symbols | CHK1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000077 | DNA damage checkpoint | IDA IEA IMP | biological_process |
| GO:0000086 | G2/M transition of mitotic cell cycle | IEA | biological_process |
| GO:0000781 | Chromosome, telomeric region | IDA | cellular_component |
| GO:0000785 | Chromatin | IEA ISS | cellular_component |
| GO:0000794 | Condensed nuclear chromosome | IDA | cellular_component |
| GO:0004674 | Protein serine/threonine kinase activity | IDA IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005634 | Nucleus | IDA IEA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005657 | Replication fork | IEA | cellular_component |
| GO:0005813 | Centrosome | IDA | cellular_component |
| GO:0005829 | Cytosol | TAS | cellular_component |
| GO:0006260 | DNA replication | TAS | biological_process |
| GO:0006281 | DNA repair | IEA IMP | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IMP | biological_process |
| GO:0006975 | DNA damage induced protein phosphorylation | IDA IEA | biological_process |
| GO:0010569 | Regulation of double-strand break repair via homologous recombination | IDA | biological_process |
| GO:0010767 | Regulation of transcription from RNA polymerase II promoter in response to UV-induced DNA damage | IEA ISS | biological_process |
| GO:0016572 | Histone phosphorylation | IDA | biological_process |
| GO:0018107 | Peptidyl-threonine phosphorylation | IDA | biological_process |
| GO:0031572 | G2 DNA damage checkpoint | IMP | biological_process |
| GO:0035402 | Histone kinase activity (H3-T11 specific) | IDA IEA | molecular_function |
| GO:0035405 | Histone-threonine phosphorylation | IDA | biological_process |
| GO:0035407 | Histone H3-T11 phosphorylation | IDA | biological_process |
| GO:0042127 | Regulation of cell proliferation | IEA | biological_process |
| GO:0045839 | Negative regulation of mitosis | IDA | biological_process |
| GO:0046602 | Regulation of mitotic centrosome separation | IDA | biological_process |
| GO:0048096 | Chromatin-mediated maintenance of transcription | IEA ISS | biological_process |
| GO:0071260 | Cellular response to mechanical stimulus | IEP | biological_process |
| GO:0071313 | Cellular response to caffeine | IEA | biological_process |
| GO:0090399 | Replicative senescence | NAS | biological_process |
| GO:2000615 | Regulation of histone H3-K9 acetylation | IEA ISS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9697189848 | 0.0018600395 | 0.9999902473 | 0.0829798305 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.2725181662 |
| GSE13712_SHEAR | Up | 0.3064003345 |
| GSE13712_STATIC | Up | 0.0908044921 |
| GSE19018 | Down | -0.1973540269 |
| GSE19899_A1 | Down | -0.5157009114 |
| GSE19899_A2 | Down | -1.4902485610 |
| PubMed_21979375_A1 | Down | -0.5487853784 |
| PubMed_21979375_A2 | Down | -1.7708514355 |
| GSE35957 | Down | -1.8614535450 |
| GSE36640 | Down | -2.3179196804 |
| GSE54402 | Down | -0.4121626469 |
| GSE9593 | Down | -0.5390138119 |
| GSE43922 | Down | -0.6353206353 |
| GSE24585 | Up | 0.2611027801 |
| GSE37065 | Down | -0.2337485340 |
| GSE28863_A1 | Down | -0.2866850025 |
| GSE28863_A2 | Up | 0.2383849312 |
| GSE28863_A3 | Down | -0.4256851657 |
| GSE28863_A4 | Up | 0.2782536313 |
| GSE48662 | Down | -1.1119098805 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-503-5p | MIMAT0002874 | MIRT000647 | Luciferase reporter assay | Functional MTI | 19956200 |
| hsa-miR-424-5p | MIMAT0001341 | MIRT000656 | Luciferase reporter assay | Functional MTI | 19956200 |
| hsa-miR-193b-3p | MIMAT0002819 | MIRT016503 | Microarray | Functional MTI (Weak) | 20304954 |
| hsa-miR-24-3p | MIMAT0000080 | MIRT030555 | Reporter assay;Western blot;qRT-PCR;Other | Functional MTI | 19748357 |
| hsa-miR-99b-5p | MIMAT0000689 | MIRT044177 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-15b-5p | MIMAT0000417 | MIRT046455 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-92a-3p | MIMAT0000092 | MIRT049764 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 21 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27181777 | In contrast, loss of Glis2 is associated with activation of checkpoint kinase 1, stabilization of p53, and induction of cell senescence |
| 26474283 | Herein we reported by western blot analysis that axitinib treatment induces a DNA damage response (DDR) initially characterized by gamma-H2AX phosphorylation and Chk1 kinase activation and at later time points by p21 overexpression in A-498 and Caki-2 RCC cells although with a different potency |
| 25801233 | After irradiation, the p21 protein was increased and Chk1 and Chk2 were activated |
| 24913980 | Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner |
| 24322375 | Induction of cellular senescence by RD occurred through activation of DNA damage response including increases in the phosphor-H2AX, inactivation of Chk1/2, and suppression of repair-related Ku70/86 and phosphor-BRCA1 in PCa cells in vitro and in vivo |
| 24272483 | Mechanistically, depletion or pharmacologic inhibition of CypB caused hyperactivation of the oncogenic RAS-mitogen-activated protein kinase pathway, induction of cellular senescence signals, and death resulting from loss of MYC, mutant p53, Chk1, and Janus-activated kinase/STAT3 signaling |
| 24023735 | We identify an upregulation of Chk1, ATM and ATR pathways in p53 negative cells and 61 other predictions obtained by knockout tests mimicking mutations |
| 23950734 | AAD inactivation impaired cell proliferation, promoted premature senescence and compromised Chk1 signalling following UV irradiation |
| 23950734 | We also show enforced TopBP1 dimerization promotes ATR-dependent Chk1 phosphorylation |
| 23272087 | This mechanism appears to preserve androgen induced autophosphorylation of ATM and phosphorylation of H2AX, lesion processing and repair pathway yet restrain ATM/CHK1/CHK2 and p53 signaling pathway |
| 22417805 | We 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 |
| 22265741 | The expression of genes related to senescence such as CHEK1 and cyclin-dependent kinase inhibitor p16(ink4a) was increased with age, however genes of apoptosis were downregulated |
| 21995812 | Differential roles for Chk1 and FANCD2 in ATR-mediated signalling for psoralen photoactivation-induced senescence |
| 21995812 | Checkpoint kinase 1 (Chk1) initiates cell cycle checkpoints, and FANCD2 is known to be involved in DNA damage-induced S-phase arrest and crosslink repair |
| 21995812 | In this study, we examined a role for Chk1 and FANCD2 as downstream effectors of ATR in senescence signalling |
| 21995812 | We demonstrate that Chk1 and FANCD2 are long-lastingly activated after psoralen photoactivation |
| 21995812 | Separate and combined reduction in Chk1 and FANCD2 expression by small interfering RNA (siRNA) preceding irradiation partly prevented the initiation of the senescence-like phenotype, whereas siRNA (Chk1 and FANCD2) transfection of senesced fibroblasts released cells from growth arrest |
| 21995812 | We observed that Chk1 and FANCD2 signal equally and additively for senescence induction, while Chk1 is predominantly responsible for maintaining persistent cell cycle arrest |
| 21995812 | In conclusion, Chk1 and FANCD2 function downstream of ATR in a non-redundant manner for the establishment and maintenance of psoralen photoactivation-induced senescence |
| 20042274 | In contrast, the inhibition of Chk1 enhanced apoptosis response in KB cell but not in A2780 |
| 18440596 | The 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 |
| 17690110 | In addition, we also found that the TWIST-mediated cellular senescence was regulated through its negative effect on p14(ARF) and subsequent suppression of MDM2/p53 and Chk1/2 DNA damage response pathways |
| 17687332 | In addition, dysfunctional telomeres might induce an ATM-independent pathway, such as ataxia telangiectasia and Rad3-related (ATR) kinase signalling, as indicated by the phosphorylation of the ATR target CHK1 in senescent cells and the response of ATM-deficient cells to telomere dysfunction |
| 16652144 | Chk1 remained phosphorylated only during the repair of double strand DNA breaks, after which Chk1 was inactivated, the G(2) arrest was suppressed, and some cells recovered their ability to proliferate |
| 16652144 | Inhibition of Chk1 by an RNAi approach resulted in an increase in cell death in p53-null cells, showing that the Chk1-dependent G(2) checkpoint protected cells that lacked a functional p53 pathway from oxidative stress |
| 16652144 | Our results indicate that oxidative stress-induced growth arrest of p53-null tumor cells cannot be equated with effective therapy owing to its reversibility and supports the concept that targeting Chk1 may enhance the effects of DNA-damaging agents on cancer progression in such tumors |
| 15760303 | After DNA damage, activation of Rad53, which together with Chk1 represents a protein kinase central to all checkpoint pathways, normally requires Rad9, a checkpoint adaptor |
| 15760303 | Rad9 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 |
| 15760303 | Finally, we report that Rad9, Mrc1, Dun1 and Chk1 are activated by phosphorylation after telomerase inactivation |
| 15610769 | X facilitates the formation of DNA damage foci around uncapped telomeres, and this in turn activates downstream kinases Chk1 and Chk2 and, eventually, p53 |
| 14608368 | We also show that senescent cells contain activated forms of the DNA damage checkpoint kinases CHK1 and CHK2 |
| 11479224 | U87MG glioma cells treated with TMZ underwent G(2)-M arrest associated with Chk1 activation and phosphorylation of both cdc25C and cdc2 |
| 11479224 | These TMZ-induced effects were inhibited by the Chk1 kinase inhibitor UCN-01 |
| 11479224 | In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death |
| 11479224 | Taken together, these results indicate that Chk1 links TMZ-induced MMR to G(2)-M arrest |
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