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Article

ATM promotes apoptosis and suppresses tumorigenesis in response to Myc.

Proceedings of the National Academy of Sciences of the United States of America - 31 Jan 2006

Pusapati Raju V, Rounbehler Robert J, Hong SungKi, Powers John T, Yan Mingshan, Kiguchi Kaoru, McArthur Mark J, Wong Paul K, Johnson David G

Abstract excerpt

Overexpression of the c-myc oncogene contributes to the development of a significant number of human cancers. In response to deregulated Myc activity, the p53 tumor suppressor is activated to promote apoptosis and inhibit tumor formation. Here we demonstrate that p53 induction in response to Myc overexpression requires the ataxia-telangiectasia mutated (ATM) kinase, a major regulator of the cellular response to...

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Identifiers

PMID: 16432227
DOI: 10.1073/pnas.0507367103
PMCID: PMC1345703

Genes

ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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