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Urinary profiles from heterozygous animals exhibited remarkably similar responses to WT before and after radiation exposure. However, genotypic differences (WT or Atm(-/-) ) were the primary driver to responses to gamma radiation.
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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.
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These data suggest that ATM and ATR are part of the cellular "infrastructure" that maintains the excitatory/inhibitory balance of the nervous system.
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ATM has a role in homology-directed repair (HDR) independent of the BRCA1-53BP1 antagonism; its HDR function can become critical in certain contexts
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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
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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
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ATM haplodeficiency decreases fibroblast senescence and vascular endothelial growth factor production and impaired angiogenesis in response to myocardial infarction, leading to accelerated heart failure.
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H2AX shows a similar influence as ATM.
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The ATM protein is a key mediator of H2O2 preconditioning.
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ATM is the primary kinase responsible for phosphorylation of Hsp90alpha after exposure ionizing radiation.
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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.
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ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed.
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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.
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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.
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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.
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WSB1 is one of the key players of early oncogenic events through ATM degradation and destruction of the tumorigenesis barrier.
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Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML, especially MLL-driven leukemias.
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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.
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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.
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The data demonstrate ATM is important for the maintenance of telomere homeostasis and the surveillance of telomere dysfunction during neurogenesis.