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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 Proteins) 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 plays a role in telomere maintenance that is independent of telomerase regulation.
Drosophila ATM and Mre11 (show MRE11A Proteins) 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 co-localizes in foci with RPA (show RPA1 Proteins) and is found in a complex with replication fork components And-1 and Mcm10 (show MCM10 Proteins). Dna2 interacts with the DSB repair and checkpoint proteins Nbs1 (show NLRP2 Proteins) and ATM.
ATM and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11 (show MRE11A Proteins)/Rad50 (show RAD50 Proteins)/Nbs1 (show NLRP2 Proteins) dependent recovery of collapsed replication forks.
ATM and ATR phosphorylate the functionally critical replication protein Mcm2 (show MCM2 Proteins) 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 Proteins) by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 (show TOPBP1 Proteins) with ATR(ATM and Rad3-related).
ATM and ATR control mitotic events in vertebrate cells by targeting CEP63 (show CEP63 Proteins) 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 Proteins)-dependent activation of ATR-ATRIP (show ATRIP Proteins) in response to double-stranded DNA breaks.
The Fanconi anemia protein FANCM is controlled by FANCD2 and the ATR/ATM pathways.
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
Characterization of ataxia telangiectasia protein.
Genomic profiling and exome sequencing identify ATM as a tumor suppressor gene and confirm that germline ATM mutations are involved in a subset of familial BC.
Of note is the recent U.S. Food and Drug Administration breakthrough therapy designation of olaparib for the treatment of BRCA1/2- or ATM-mutated metastatic castration-resistant prostate cancer. The implications of this new knowledge for clinical practice now and in the future are discussed.
Study identifies germline variants in ATM gene in a subset of patients with early-onset breast cancer and confirms ATM as breast cancer susceptibility gene.
Our results suggest the identification of ATM mutations in CLL patients with 11q deletion at diagnosis is clinically relevant and predicts disease progression, poor response to the treatment, and reduced OS independent of other molecular prognostic factors.
WSB1 (show WSB1 Proteins) is one of the key players of early oncogenic events through ATM degradation and destruction of the tumorigenesis barrier.
We conclude that an ATM-ATX axis interconnects double-strand breaks with silica-induced inflammation and propagates these effects in epithelial cells
ATM mutation prevalence in Spanish population highlights the importance of considering ATM pathogenic variants linked to breast cancer susceptibility.
Collectively, these data indicated that ATR (show ANTXR1 Proteins) or ATM inhibition represent potential therapeutic strategies for the treatment of AML (show RUNX1 Proteins), especially MLL (show MLL Proteins)-driven leukemias.
NOTCH1 (show NOTCH1 Proteins) inhibits activation of ATM by impairing the formation of an ATM-FOXO3a (show FOXO3 Proteins)-KAT5 (show KAT5 Proteins) complex.
No strong correlation was observed between ATM mutation and function. Therefore, mutation status may not be taken as an indicator of ATM function. Rather, a direct assay of the kinase activity should be used in the development of therapies.
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 Proteins) activation in bovine aortic endothelial cells is regulated by ATM and HSP90 (show HSP90 Proteins)
Baf60b (show SMARCD2 Proteins), a member of the SWI/SNF chromatin remodeling complex (show SMARCA2 Proteins), links chromatin opening to ATM activation by facilitating ATM recruitment to the open chromatin regions of a panel of hepatic gene loci.
Results demonstrate that alterations in ATM levels are responsible for pronounced and anticipated GABAergic development and function. Since GABA transmission is strongly linked to the correct brain development and plasticity, this study lays basics for both a more clear comprehension of mechanisms associated with brain development.
These data indicate that defective Atm reduces the redox homeostasis of the testis and genetic integrity of sperm by regulating glutathione levels independently from G6PDH (show G6PD Proteins) activity.
Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML (show RUNX1 Proteins), especially MLL (show MLL Proteins)-driven leukemias.
Data show that Tp53 (show TP53 Proteins)- and Atm-defective Chronic lymphocytic leukemia (CLL) mimicking the high-risk form of human disease and that Atm-deficient CLL is sensitive to PARP1 (show PARP1 Proteins) inhibition.
Depletion of H3K9ac in embryonic stem cells by suppression of monocytic leukemia zinc finger protein (MOZ) acetyltransferase improved ATM activation, DNA repair, diminished irradiation-induced apoptosis, and enhanced clonogenic survival.
The data demonstrate ATM is important for the maintenance of telomere homeostasis and the surveillance of telomere dysfunction during neurogenesis.
DNA damage induces a kinetochore-based ATM/ATR-independent spindle assembly checkpoint arrest.
The SAGA deubiquitinase activity was required for optimal irradiation-induced gammaH2AX (show H2AFX Proteins) formation, and failure to remove H2BK120ub inhibits ATM- and DNAPK (show PRKDC Proteins)-induced gammaH2AX (show H2AFX Proteins) formation.
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