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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...

Topics

Adenovirus E1A Proteins
Animals
Apoptosis
Cell Transformation, Neoplastic
Cells, Cultured
DNA
DNA Damage
Genes, ras
Kidney
Mutation
Rats
Tumor Suppressor Protein p53

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

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

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7623844-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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