HCSGD entry for ATR
1. General information
| Official gene symbol | ATR |
|---|---|
| Entrez ID | 545 |
| Gene full name | ataxia telangiectasia and Rad3 related |
| Other gene symbols | FCTCS FRP1 MEC1 SCKL SCKL1 |
| 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 | biological_process |
| GO:0001741 | XY body | IEA | cellular_component |
| GO:0003677 | DNA binding | IEA | molecular_function |
| GO:0004672 | Protein kinase activity | IDA | molecular_function |
| GO:0004674 | Protein serine/threonine kinase activity | IDA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005694 | Chromosome | ISS | cellular_component |
| GO:0006260 | DNA replication | TAS | biological_process |
| GO:0006281 | DNA repair | TAS | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | TAS | biological_process |
| GO:0007049 | Cell cycle | TAS | biological_process |
| GO:0007275 | Multicellular organismal development | TAS | biological_process |
| GO:0008156 | Negative regulation of DNA replication | IMP | biological_process |
| GO:0016301 | Kinase activity | IEA | molecular_function |
| GO:0016605 | PML body | IDA | cellular_component |
| GO:0016773 | Phosphotransferase activity, alcohol group as acceptor | IEA | molecular_function |
| GO:0018105 | Peptidyl-serine phosphorylation | IDA | biological_process |
| GO:0032405 | MutLalpha complex binding | IDA | molecular_function |
| GO:0032407 | MutSalpha complex binding | IDA | molecular_function |
| GO:0034644 | Cellular response to UV | IMP | biological_process |
| GO:0042493 | Response to drug | IEA | biological_process |
| GO:0043393 | Regulation of protein binding | IEA | biological_process |
| GO:0043517 | Positive regulation of DNA damage response, signal transduction by p53 class mediator | IMP | biological_process |
| GO:0046777 | Protein autophosphorylation | IDA | biological_process |
| GO:0071480 | Cellular response to gamma radiation | IDA | biological_process |
| GO:0090399 | Replicative senescence | IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.1929329053 | 0.2574984461 | 0.8520208690 | 0.9725315352 |
- 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 | Up | 0.5379631411 |
| GSE13712_SHEAR | Down | -0.0332932184 |
| GSE13712_STATIC | Up | 0.0343640985 |
| GSE19018 | Down | -0.4233456365 |
| GSE19899_A1 | Up | 0.1805886327 |
| GSE19899_A2 | Up | 0.0201020661 |
| PubMed_21979375_A1 | Up | 0.5111827303 |
| PubMed_21979375_A2 | Up | 0.5268223476 |
| GSE35957 | Down | -0.0245876192 |
| GSE36640 | Down | -0.0032330852 |
| GSE54402 | Up | 0.3090907073 |
| GSE9593 | Down | -0.3166948052 |
| GSE43922 | Up | 0.1966553546 |
| GSE24585 | Down | -0.4693465110 |
| GSE37065 | Up | 0.0602183671 |
| GSE28863_A1 | Up | 0.1610746586 |
| GSE28863_A2 | Up | 0.6431414968 |
| GSE28863_A3 | Down | -0.8316426295 |
| GSE28863_A4 | Down | -0.2668129182 |
| GSE48662 | Down | -0.3968840352 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-let-7f-5p | MIMAT0000067 | MIRT051394 | 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: 22 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26871293 | These effects of As2O3 trigger an extensive DNA damage response at the telomere, which includes up-regulation of ATM, ATR, 53BP1, gamma-H2AX and Mer11, in parallel with telomere fusion and 3'-overhang degradation |
| 26404840 | GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a) |
| 25573782 | RESULTS: We define a discrete, logical model encompassing ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related) pathways activation upon DNA damage, as well as G1/S checkpoint main components |
| 24937130 | Loss of ATM activity, either by genomic mutation (ATM-deficient fibroblasts from an ataxia telangiectasia patient) or by administration of a chemical inhibitor (AAI, an inhibitor of ATM and ATR), blocks IGF-1-sCLU expression in senescent cells |
| 24091330 | In contrast to p16(INK4a), deletion of p21 did not activate ATR, rescued proliferative defects in Pot1bDelta/Delta hematopoietic cells, and significantly increased organismal lifespan |
| 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 | ATR activation is dependent on temporal and spatial interactions with partner proteins |
| 23950734 | In metazoans, only TopBP1 has been identified as a direct ATR activator |
| 23950734 | Depletion-replacement approaches suggest the TopBP1-AAD is both sufficient and necessary for ATR activation |
| 23950734 | Our data suggest that, unlike the yeast models, the TopBP1-AAD is the major activator of ATR, sustaining cell proliferation and embryonic development |
| 23676215 | Replication stress (RS) is a source of DNA damage that has been linked to cancer and aging, which is suppressed by the ATR kinase |
| 23676215 | In mice, reduced ATR levels in a model of the ATR-Seckel syndrome lead to RS and accelerated aging |
| 22516260 | Here, we show induction of a fail-safe mechanism mediated by the DNA damage response (DDR) machinery that results in activation of the ATR/ATM-Chk1/Chk2-p53/p21(CIP1) checkpoint and cellular senescence at early stages of cellular transformation caused by a regulatable MLL-ENL-ERtm in mice |
| 21995812 | Previously, we have shown that DNA interstrand crosslink formation by photoactivated psoralens induces a senescent phenotype in primary fibroblasts that is mediated by Ataxia telangiectasia-mutated and Rad3-related (ATR) kinase |
| 21995812 | In this study, we examined a role for Chk1 and FANCD2 as downstream effectors of ATR in senescence signalling |
| 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 |
| 21336312 | Oncogene-induced SAHF formation depends on DNA replication and ATR (ataxia telangiectasia and Rad3-related) |
| 21336312 | Oncogene-induced SAHF formation depends on DNA replication and ATR (ataxia telangiectasia and Rad3-related) |
| 20084458 | Ataxia-Telangiectasia and Rad3 related kinase (ATR) is a major gatekeeper of genomic stability and has been the subject of exhaustive study in the context of cell cycle progression and senescence as a DNA damage-induced response |
| 20084458 | In light of the above, we investigate the RNA processing machinery in senescent fibroblasts as opposed to young, either exponentially proliferating or quiescent, further focusing on the distribution and localization of active, phosphorylated ATR at ser428 |
| 19324671 | However, following ATM kinase inhibition using a specific ATM inhibitor, we observed a significant increase in ATM and ataxia-telangiectasia and Rad3 related transcription |
| 19098271 | Drug-induced DNAM-1 and NKG2D ligand expression was abolished after treatment with the ATM (ataxia telangiectasia mutated) and ATR (ATM- and RAD3-related) pharmacologic inhibitors caffeine and KU-55933, and was preferentially associated with senescent cells arrested in the G2 phase of the cell cycle |
| 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 |
| 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 |
| 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 |
| 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 |
| 17687332 | Here we show that damaged mammalian telomeres can activate both ATM and ATR and address the mechanism by which the shelterin complex represses these two important DNA damage signalling pathways |
| 17687332 | Unexpectedly, we found that either ATM or ATR signalling is required for efficient non-homologous end-joining of dysfunctional telomeres |
| 16767085 | Here we show that the intrinsic 'senescence clock' can be reset in a reversible manner by selective modulation of the ataxia telangiectasia-mutated (ATM) protein and ATM- and Rad3-related (ATR) protein with a small molecule, CGK733 |
| 16767085 | CGK733 inhibits ATM and ATR kinase activities and blocks their checkpoint signaling pathways with great selectivity |
| 16767085 | Consistently, siRNA-mediated knockdown of ATM and ATR induced the proliferation of senescent cells, although with lesser efficiency than CGK733 |
| 16767085 | These results might reflect the specific targeting of the kinase activities of ATM and ATR by CGK733 without affecting any other domains required for cell proliferation |
| 16436511 | Senescence of human fibroblasts after psoralen photoactivation is mediated by ATR kinase and persistent DNA damage foci at telomeres |
| 16436511 | In the present study, we demonstrate that senescence after PUVA depends on DNA interstrand cross-link (ICL) formation that activates ATR kinase |
| 16436511 | ATR is necessary for the manifestation and maintenance of the senescent phenotype, because depletion of ATR expression before PUVA prevents induction of senescence, and reduction of ATR expression in PUVA-senesced fibroblasts releases cells from growth arrest |
| 16436511 | ATR is necessary for the manifestation and maintenance of the senescent phenotype, because depletion of ATR expression before PUVA prevents induction of senescence, and reduction of ATR expression in PUVA-senesced fibroblasts releases cells from growth arrest |
| 16436511 | ATR is necessary for the manifestation and maintenance of the senescent phenotype, because depletion of ATR expression before PUVA prevents induction of senescence, and reduction of ATR expression in PUVA-senesced fibroblasts releases cells from growth arrest |
| 16436511 | After PUVA, ATR and gamma-H2AX colocalize in multiple nuclear foci |
| 16436511 | After several days, only few predominantly telomere-localized foci persist and telomeric DNA can be coimmunoprecipitated with ATR from PUVA-senesced fibroblasts |
| 16436511 | We thus identify ATR as a novel mediator of telomere-dependent senescence in response to ICL induced by photoactivated psoralens |
| 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 |
| 15610769 | Second, the signalling pathway connecting telomere uncapping and replicative senescence appears to be the same as the one that is activated by DNA damage: uncapped telomeres activate signalling cascades involving the protein kinases ATM, ATR and, possibly, DNA-PK |
| 15149599 | ATR kinase appears to play a minor role in normal cells but in the absence of ATM elicited a delayed G2 phase arrest |
| 12072449 | Regulation of genome stability by TEL1 and MEC1, yeast homologs of the mammalian ATM and ATR genes |
| 12072449 | Regulation of genome stability by TEL1 and MEC1, yeast homologs of the mammalian ATM and ATR genes |
| 12072449 | In the yeast Saccharomyces cerevisiae, two members of this family, TEL1 and MEC1, have functionally redundant roles in both DNA damage repair and telomere length regulation |
| 12072449 | Similar chromosome rearrangements have been detected in mammalian cells with mutations in ATM (related to TEL1) and ATR (related to MEC1) and in mammalian cells that approach cell crisis |
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