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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 (zeige TPT1 Proteine) 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 (zeige MRE11A Proteine) 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 (zeige RPA1 Proteine) and is found in a complex with replication fork components And-1 and Mcm10 (zeige MCM10 Proteine). Dna2 interacts with the DSB repair and checkpoint proteins Nbs1 (zeige NLRP2 Proteine) and ATM.
ATM and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11 (zeige MRE11A Proteine)/Rad50 (zeige RAD50 Proteine)/Nbs1 (zeige NLRP2 Proteine) dependent recovery of collapsed replication forks.
ATM and ATR phosphorylate the functionally critical replication protein Mcm2 (zeige MCM2 Proteine) 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 (zeige TOPBP1 Proteine) by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 (zeige TOPBP1 Proteine) with ATR(ATM and Rad3-related).
ATM and ATR control mitotic events in vertebrate cells by targeting CEP63 (zeige CEP63 Proteine) and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1 (zeige TOPBP1 Proteine)-dependent activation of ATR-ATRIP (zeige ATRIP Proteine) 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.
Moreover, under positive p53 expression, low expression of ATM was highly predictive of poor survival in ACC (p=0.017). CONCLUSION: These data indicate that combined assessment of ATM and p53 expression can serve as a useful prognostic marker for assessing survival rate in patients with ACC [Adenoid cystic carcinoma] of the salivary glands.
results reveal how alterations in FBXO31 (zeige FBXO5 Proteine) phosphorylation, mediated by AKT (zeige AKT1 Proteine) and ATM, underlie physiological regulation of FBXO31 (zeige FBXO5 Proteine) levels in unstressed and genotoxically stressed cells
Combination of T-cell lymphoma-1 (zeige TCL1A Proteine) protein (TCL1 (zeige TCL1A Proteine))-overexpression and damaging ataxia telangiectasia mutated protein (ATM) functionally synergistically contribute to T-cell prolymphocytic leukemia (T-PLL) specific phenotype of impaired DNA damage processing.
These findings suggested that the ATM/p21 (zeige CDKN1A Proteine) pathway directly participated in the LDIR-induced cell proliferation inhibition in p53null type prostate tumor cells, whereas this mechanism was absent in normal prostate cells. Thus, p53 (zeige TP53 Proteine) may affect cell stability following LDIR, and plays a crucial role in regulating the ATM/p21 (zeige CDKN1A Proteine) pathway activated by LDIR.
Truncating variants in PALB2, ATM and CHEK2 , but not XRCC2 were associated with increased breast cancer risk.
our results identify a novel link between XRRA1 and the ATM/CHK1 (zeige CHEK1 Proteine)/2 pathway and suggest that XRRA1 is involved in a DNA damage response that drives radio- and chemoresistance by regulating the ATM/CHK1 (zeige CHEK1 Proteine)/2 pathway.
A target-enrichment next-generation sequencing strategy on 28 Spanish ataxia-telangiectasia patients identified gene variants affecting function in 54 of the 56 alleles analyzed. 28 ATM gene mutations were found, of which 10 have not been reported. A total of 171 gene variants not affecting function were also found; 22 predispose to disease. All Roma patients were homozygous for the same mutation and share haplotype H3.
Variations in the ATM gene and its encoding product, the ATM protein, are found to affect the pathogenesis, development, response to treatment and prognosis of lung cancer
The polymorphisms rs664143 and rs664677 of ATM are associated with lung cancer occurrence
These evidences suggest that NBS1 (zeige NBN Proteine) is regulated by two kind of mechanisms: complex formation dependent on ATM, and protein degradation mediated by an unknown MG132-resistant pathway.
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 (zeige NOS3 Proteine) activation in bovine aortic endothelial cells is regulated by ATM and HSP90 (zeige HSP90 Proteine)
SOD2 (zeige SOD2 Proteine) expression is ATM- and RelA (zeige NFkBP65 Proteine)-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2 (zeige SOD2 Proteine).
These data suggest that ATM and ATR are part of the cellular "infrastructure" that maintains the excitatory/inhibitory balance of the nervous system.
ATM has a role in homology-directed repair (HDR (zeige GATA3 Proteine)) independent of the BRCA1 (zeige BRCA1 Proteine)-53BP1 (zeige TP53BP1 Proteine) antagonism; its HDR (zeige GATA3 Proteine) function can become critical in certain contexts
intestinal tuft cells play an important role in regulating the ATM mediated DNA damage response, for epithelial cell survival/self-renewal via a Dclk1 (zeige DCLK1 Proteine) dependent mechanism
in the Atm(-/-) MEFs, the same Radiofrequency electromagnetic fields exposure for 12 h induced both SSBs and double-strand breaks and activated the two repair processes, which also reduced the DNA damage to less than the control level after prolonged exposure. The observed phenomenon is similar to the hormesis of a toxic substance at a low dose
ATM haplodeficiency decreases fibroblast senescence and vascular endothelial growth factor (zeige VEGF Proteine) production and impaired angiogenesis in response to myocardial infarction, leading to accelerated heart failure.
H2AX (zeige H2AFX Proteine) shows a similar influence as ATM.
The ATM protein is a key mediator of H2O2 preconditioning.
ATM is the primary kinase responsible for phosphorylation of Hsp90alpha (zeige HSP90AA2 Proteine) after exposure ionizing radiation.
These findings define an antagonistic function of ATM and MAPK7 (zeige MAPK7 Proteine) in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 (zeige MAPK7 Proteine) inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
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