p63, cellular senescence and tumor development

Guo, X. C., Mills, A. A. (February 2007) p63, cellular senescence and tumor development. Cell Cycle, 6 (3). pp. 305-11. ISSN 1538-4101

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URL: https://www.ncbi.nlm.nih.gov/pubmed/17224650
DOI: 10.4161/cc.6.3.3794

Abstract

Deficiency of p63, a p53-related protein, causes severe defects in epithelial morphogenesis. Studies of p63-compromised mouse models reveal that p63 deficiency induces cellular senescence both in cultured cells and in vivo, through regulation p19(Arf)/p53 and p16(Ink4a)/Rb pathways. An extensive tumor study of p63-compromised mice demonstrated that p63 deficiency does not predispose to, but rather protects from, tumor development. These findings further implicate p63 as a negative regulator of the tumor suppressive mechanism of cellular senescence.

Item Type: Paper
Uncontrolled Keywords: p63 senescence tumorigenesis oncogene tumor suppressor animal model P53-FAMILY MEMBERS P63 P53 TARGET GENES DIFFERENTIAL REGULATION ONCOGENIC RAS IN-VIVO TRANSCRIPTIONAL ACTIVITY P53-DEPENDENT APOPTOSIS REPLICATIVE SENESCENCE PREMATURE SENESCENCE NUCLEAR ACCUMULATION
Subjects: diseases & disorders > cancer
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
organism description > animal > mammal > rodent > mouse
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p53
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p63
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > senescence
CSHL Authors:
Communities: CSHL labs > Mills lab
Depositing User: CSHL Librarian
Date: February 2007
Date Deposited: 15 Nov 2011 14:28
Last Modified: 02 Feb 2017 17:06
Related URLs:
URI: http://repository.cshl.edu/id/eprint/23022

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