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our data indicate that ATR and ATM are both needed for intestinal stem cell maintenance and proliferation; ATR seems to play a bigger role than does ATM.
TCTP (show TPT1 ELISA Kits) has a role in regulating ATM activity to control genome stability and organ development in Drosophila melanogaster
A stringent requirement for the conserved function of Ataxia Telangiectasia Mutated (ATM) in telomere protection during early embryonic development, is identified.
ATM is primarily required for the meiotic DSB repair response, which includes functions in DNA damage repair and negative feedback control over the level of programmed DSBs during meiosis.
Molecular genetic characterization of Drosophila ATM conserved functional domains.
ATM checkpoint kinase (show ATR ELISA Kits) plays a role in telomere maintenance that is independent of telomerase regulation.
Drosophila ATM and Mre11 (show MRE11A ELISA Kits) are essential for the G2/M checkpoint induced by low-dose irradiation.
Results suggest that ATM and ATR protect telomere integrity by safeguarding chromatin architecture that favors the loading of telomere-elongating, capping, and silencing proteins.
Dna2 (show DNA2 ELISA Kits) co-localizes in foci with RPA (show RPA1 ELISA Kits) and is found in a complex with replication fork components And-1 and Mcm10 (show MCM10 ELISA Kits). Dna2 (show DNA2 ELISA Kits) interacts with the DSB repair and checkpoint proteins Nbs1 (show NLRP2 ELISA Kits) and ATM.
ATM and ATR (show ATR ELISA Kits) prevent accumulation of chromosomal abnormalities by promoting Mre11 (show MRE11A ELISA Kits)/Rad50 (show RAD50 ELISA Kits)/Nbs1 (show NLRP2 ELISA Kits) dependent recovery of collapsed replication forks.
ATM and ATR (show ATR ELISA Kits) phosphorylate the functionally critical replication protein Mcm2 (show MCM2 ELISA Kits) during both DNA damage and replication checkpoint responses in Xenopus egg extracts
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
Data show that ATM (ataxia-telangiectasia mutated) regulates Xenopus TopBP1 (show TOPBP1 ELISA Kits) by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 (show TOPBP1 ELISA Kits) with ATR (show ATR ELISA Kits)(ATM and Rad3-related).
ATM and ATR (show ATR ELISA Kits) control mitotic events in vertebrate cells by targeting CEP63 (show CEP63 ELISA Kits) and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1 (show TOPBP1 ELISA Kits)-dependent activation of ATR (show ATR ELISA Kits)-ATRIP (show ATRIP ELISA Kits) in response to double-stranded DNA breaks.
The Fanconi anemia protein FANCM (show FANCM ELISA Kits) is controlled by FANCD2 (show FANCD2 ELISA Kits) and the ATR (show ATR ELISA Kits)/ATM pathways.
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
Characterization of ataxia telangiectasia protein.
ASF1a (show ASF1A ELISA Kits) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 (show MDC1 ELISA Kits) by ATM at double-strand breaks.
ectopic expression of Gene 33 triggers DNA damage response in an ATM serine/threonine kinase (ATM)-dependent fashion and through pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
We demonstrate that, in breast cancer cells, ATM and ATG4C (show ATG4C ELISA Kits) are essential drivers of mammosphere formation, suggesting that their targeting may improve current approaches to eradicate breast cancer cells with a stem-like phenotype.
ATM-reactive oxygen species-iNOS (show NOS2 ELISA Kits) axis regulates nitric oxide mediated cellular senescence.
DNA-PKcs (show PRKDC ELISA Kits), which is integral to the non-homologous end joining pathway, negatively regulates ATM activity through phosphorylation of ATM.
The data suggest that pre-B cells are endowed with a protective mechanism that reduces the risk for aberrant recombinations and chromosomal translocations when exposed to DNA damage, involving the ATM-dependent regulation of FOXO1 (show FOXO1 ELISA Kits) binding to the Erag enhancer region.
Data suggest HSP90AA1-dependent regulation of ATM-NBN-CHK2 and ATR-CHK1 axes influences cells capability to repair double-stranded DNA damage; mechanisms include phosphorylation, polyubiquitination, and proteasomal degradation/proteolysis. (HSP90AA1 = heat shock protein 90kDa alpha; ATM = ataxia telangiectasia mutated protein; NBN = nibrin; CHK = checkpoint kinase; ATR = ataxia telangiectasia and Rad3 related kinase)
DNA damage-induced ATM- and Rad-3-related (ATR (show ANTXR1 ELISA Kits)) kinase activation in non-replicating cells is regulated by the XPB (show GTF2H5 ELISA Kits) subunit of transcription factor IIH (TFIIH (show GTF2H1 ELISA Kits))
variants in ATM were associated with moderate risks of breast cancer.
We report that endogenous huntingtin (show HTT ELISA Kits) protein directly participates in oxidative DNA damage repair. Using novel chromobodies to detect endogenous human huntingtin (show HTT ELISA Kits) in live cells, we show that localization of huntingtin (show HTT ELISA Kits) to DNA damage sites is dependent on the kinase activity of ataxia telangiectasia mutated (ATM) protein.
Ataxia telangiectasia (AT) is a progressive multisystem disorder caused by mutations in the AT-mutated (ATM) gene. We engineered a novel porcine model of AT
ATM influenced the meiotic and cytoplasmic maturation of porcine oocytes.
ATM plays critical role in arsenite induced G2/M phase arrest in aortic endothelial cells possibly via regulation of checkpoint signaling molecules.
radiation-induced eNOS (show NOS3 ELISA Kits) activation in bovine aortic endothelial cells is regulated by ATM and HSP90 (show HSP90 ELISA Kits)
The SAGA deubiquitinase activity was required for optimal irradiation-induced gammaH2AX (show H2AFX ELISA Kits) formation, and failure to remove H2BK120ub inhibits ATM- and DNAPK (show PRKDC ELISA Kits)-induced gammaH2AX (show H2AFX ELISA Kits) formation.
ATM expression by peritoneal B cells is required to facilitate viral reactivation during long-term infection. Thus, this study defines a proviral role of B cell-specific ATM expression during chronic gammaherpesvirus infection.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (show TRAF1 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits)-regulated apoptosis and the p53 (show TP53 ELISA Kits)/PCNA (show PCNA ELISA Kits)- and ATM/ATR (show ATR ELISA Kits)-Chk1 (show CHEK1 ELISA Kits)/2-controlled DNA-damage response pathways.
this study shows that Atm-/- mice are more susceptible to pulmonary Streptococcus pneumoniae infection in a manner consistent with inflammasome defects
This study show that like ataxia telangiectasia cells, ISG15 (show ISG15 ELISA Kits) is elevated in Atm-deficient mouse cerebellums.
This study identifies attenuation of type I interferon (show IFNA ELISA Kits) responses as the primary mechanism underlying proviral function of ATM during gammaherpesvirus infection.
Mutant IDH1 (show IDH1 ELISA Kits) downregulates the DNA damage (DD) sensor ATM by altering histone methylation, leading to impaired DNA repair, increased sensitivity to DD, and reduced HSC (show FUT1 ELISA Kits) self-renewal, independent of TET2 (show TET2 ELISA Kits).
USP7 (show USP7 ELISA Kits) inhibition is selectively cytotoxic to CLL cells independently of ATM and p53 (show TP53 ELISA Kits) and synergizes with chemotherapy.
Fractionated exposure to low doses of X-rays resulted in accumulation of DNA damage in the murine spleen and induction of apoptotic response in p53 (show TP53 ELISA Kits)/Atm-independent manner. Further studies are needed to understand the outcomes and molecular mechanisms underlying cellular responses and early induction of p38 (show CRK ELISA Kits) in response to prolonged exposure to IR.
ATM, ATR (show ATR ELISA Kits) and DNA-PKcs (show PRKDC ELISA Kits) have unique and essential roles during the DNA damage response in the nervous system.
The protein encoded by this gene belongs to the PI3/PI4-kinase family. This protein is an important cell cycle checkpoint kinase that phosphorylates\; thus, it functions as a regulator of a wide variety of downstream proteins, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1. This protein and the closely related kinase ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. Mutations in this gene are associated with ataxia telangiectasia, an autosomal recessive disorder.
, ataxia telangiectasia mutated
, ataxia telengiesctasia mutated
, ataxia-telangiectasia mutated
, drosophila ATM
, ataxia telangiectasia mutated (includes complementation groups A, C and D)
, ataxia telangiectasia mutated protein
, serine-protein kinase ATM-like
, ataxia telangiectasia mutated (atm)
, A-T mutated
, AT mutated
, TEL1, telomere maintenance 1, homolog
, serine-protein kinase ATM
, Ataxia telangiectasia gene mutated in human beings
, ataxia telangiectasia mutated homolog
, A-T mutated homolog
, ATM (ataxia telangiectasia mutated)
, ataxia telangiectasia gene mutated in human beings