Journal
AUTOPHAGY
Volume 8, Issue 5, Pages 840-841Publisher
LANDES BIOSCIENCE
DOI: 10.4161/auto.19693
Keywords
Ataxia Telangiectasia Mutated gene; mitochondrial dysfunction; PARKIN; BECN1; mitophagy
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Funding
- NCI NIH HHS [R01 CA157216] Funding Source: Medline
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The various pathologies in ataxia telangiectasia (A-T) patients including T-cell lymphomagenesis have been attributed to defects in the DNA damage response pathway because ATM, the gene mutated in this disease, is a key mediator of this process. Analysis of Atm-deficient thymocytes in mice reveals that the absence of this gene results in altered mitochondrial homeostasis, a phenomenon that appears to result from abnormal mitophagy engagement. Interestingly, allelic loss of the autophagic gene Becn1 delays tumorigenesis in Atm-null mice presumably by reversing the mitochondrial abnormalities and not by improving the DNA damage response (DDR) pathway. Thus, ATM plays a critical role in modulating mitochondrial homeostasis perhaps by regulating mitophagy.
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