Cellular and molecular advances in elucidating p53 function

Jerry W. Shay, Harold Werbin, Walter D. Funk, Woodring E. Wright

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The finding that in many human tumors there is allelic loss and/or mutations in p53, in combination with recognition that these events may play a role in multi-stage carcinogenesis, has focused considerable interest on this gene. To help keep abreast of this rapidly expanding field, recent experiments on the role and potential regulation of p53 are described: these include discussions of p53 as an anti-proliferative agent, the p53 mutations found in human tumors and tumor cell lines, the conformational states of p53 phosphorylation of p53 by p34cdc2, and signals for the nuclear localization of p53. p53 may act as a transcriptional activator and the specific DNA sequences to which p53 protein binds are also discussed as is the importance of abrogation of p53 function in overcoming cellular senescence.

Original languageEnglish (US)
Pages (from-to)163-171
Number of pages9
JournalMutation Research/Reviews in Genetic Toxicology
Volume277
Issue number2
DOIs
StatePublished - 1992

Fingerprint

Tumors
Nuclear Localization Signals
Mutation
Cell Aging
Loss of Heterozygosity
Tumor Cell Line
Neoplasms
Carcinogenesis
Phosphorylation
DNA sequences
Genes
Cells
Proteins
Experiments

Keywords

  • Allelic loss
  • Human tumors
  • Multi-stage carcinogenesis
  • p53 function

ASJC Scopus subject areas

  • Genetics
  • Toxicology

Cite this

Cellular and molecular advances in elucidating p53 function. / Shay, Jerry W.; Werbin, Harold; Funk, Walter D.; Wright, Woodring E.

In: Mutation Research/Reviews in Genetic Toxicology, Vol. 277, No. 2, 1992, p. 163-171.

Research output: Contribution to journalArticle

Shay, Jerry W. ; Werbin, Harold ; Funk, Walter D. ; Wright, Woodring E. / Cellular and molecular advances in elucidating p53 function. In: Mutation Research/Reviews in Genetic Toxicology. 1992 ; Vol. 277, No. 2. pp. 163-171.
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