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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 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 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 and is found in a complex with replication fork components And-1 and Mcm10. Dna2 interacts with the DSB repair and checkpoint proteins Nbs1 and ATM.
ATM and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11/Rad50/Nbs1 dependent recovery of collapsed replication forks.
ATM and ATR phosphorylate the functionally critical replication protein Mcm2 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 by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 with ATR(ATM and Rad3-related).
ATM and ATR control mitotic events in vertebrate cells by targeting CEP63 and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1-dependent activation of ATR-ATRIP 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.
High ATM expression is associated with chemotherapeutic resistance in gastric cancer.
No significant association of ATM rs11212592 with lung cancer was found in five genetic models in Chinese population. Haplotypes consisting of PPP1R13L rs1970764 and ATM rs11212592 may be associated with lung cancer.
The miR-449a/ATDC axis plays an important role in the development and progression of pancreatic cancer.
The ATM structure shows the detailed topology of the regulator-interacting N-terminal helical solenoid. The ATM conformational dynamics shown by the structures represent an important step in understanding the enzyme regulation.
ATM and CDK2 control the chromatin remodeling activity of CSB in the regulation of double strand break repair pathway choice.
Data suggest that ataxia telangiectasia mutated protein (ATM) mutational status in lung cancer is a mechanistic biomarker for MEK inhibitor response.
Data suggest a close association between the nonfunctionality of ATM/p53 pathway and accumulation of p27Kip1 in chronic lymphocytic leukemia (CLL) cells in response to DNA damage.
Letter: BRCA2- and ATM-mutated prostate cancer sensitive to high dose testosterone.
Radiation-activated ataxia-telangiectasia mutated kinase/p38 signaling positively contributed to the nucleus to cytosol translocation of HuR.
No significant differences were presented in DNA methylation levels of RASSF1A and ATM between the sporadic breast cancer cases and the healthy controls.
The ATM rs189037, rs664677 and rs664143 gene polymorphisms are risk factors for lung cancer, while the ATM rs189037 variant was significantly associated with radiation-induced pneumonitis risk. [meta-analysis]
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 phosphorylation, mediated by AKT and ATM, underlie physiological regulation of FBXO31 levels in unstressed and genotoxically stressed cells
Combination of T-cell lymphoma-1 protein (TCL1)-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 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 may affect cell stability following LDIR, and plays a crucial role in regulating the ATM/p21 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/CHK1/2 pathway and suggest that XRRA1 is involved in a DNA damage response that drives radio- and chemoresistance by regulating the ATM/CHK1/2 pathway.
In the Title.
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
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.
The extensive alternative splicing of the pATM gene resembles the complex splicing observed in the hATM and could provide insights for differences observed between mice and humans with regards to the onset of A-T
radiation-induced eNOS activation in bovine aortic endothelial cells is regulated by ATM and HSP90
SOD2 expression is ATM- and RelA-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.
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) independent of the BRCA1-53BP1 antagonism; its HDR 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 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 production and impaired angiogenesis in response to myocardial infarction, leading to accelerated heart failure.
H2AX 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 after exposure ionizing radiation.
These findings define an antagonistic function of ATM and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed.
Baf60b, a member of the SWI/SNF chromatin remodeling complex, 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 activity.
WSB1 is one of the key players of early oncogenic events through ATM degradation and destruction of the tumorigenesis barrier.
Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML, especially MLL-driven leukemias.
Data show that Tp53- and Atm-defective Chronic lymphocytic leukemia (CLL) mimicking the high-risk form of human disease and that Atm-deficient CLL is sensitive to PARP1 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 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