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Article

Activated H-ras rescues E1A-induced apoptosis and cooperates with E1A to overcome p53-dependent growth arrest.

Molecular and cellular biology - 1 Aug 1995

Lin H J, Eviner V, Prendergast G C, White E

Abstract excerpt

The adenovirus E1A oncogene products stimulate DNA synthesis and cell proliferation but fail to transform primary baby rat kidney (BRK) cells because of the induction of p53-mediated programmed cell death (apoptosis). Overexpression of dominant mutant p53 (to abrogate wild-type p53 function) or introduction of apoptosis inhibitors, such as adenovirus E1B 19K or Bcl-2 oncoproteins, prevents E1A-induced apoptosis...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 7623844
DOI: 10.1128/MCB.15.8.4536
PMCID: PMC230693

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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