E1A signaling to p53 involves the p19(ARF) tumor suppressor

de Stanchina, E., McCurrach, M. E., Zindy, F., Shieh, S. Y., Ferbeyre, G., Samuelson, A. V., Prives, C., Roussel, M. F., Sherr, C. J., Lowe, S. W. (August 1998) E1A signaling to p53 involves the p19(ARF) tumor suppressor. Genes Dev, 12 (15). pp. 2434-42. ISSN 0890-9369 (Print)

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Abstract

The adenovirus E1A oncogene activates p53 through a signaling pathway involving the retinoblastoma protein and the tumor suppressor p19(ARF). The ability of E1A to induce p53 and its transcriptional targets is severely compromised in ARF-null cells, which remain resistant to apoptosis following serum depletion or adriamycin treatment. Reintroduction of p19(ARF) restores p53 accumulation and resensitizes ARF-null cells to apoptotic signals. Therefore, p19(ARF) functions as part of a p53-dependent failsafe mechanism to counter uncontrolled proliferation. Synergistic effects between the p19(ARF) and DNA damage pathways in inducing p53 may contribute to E1A's ability to enhance radio- and chemosensitivity.

Item Type: Paper
Uncontrolled Keywords: Adenovirus E1A Proteins genetics Animals Apoptosis genetics Cell Division genetics Cells Cultured DNA Damage Gene Expression Regulation Genes Tumor Suppressor Genes Viral Genes p53 Mice Mice Knockout Proteins genetics Signal Transduction Tumor Suppressor Protein p14ARF
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > E1A protein
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > oncogene
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p53
CSHL Authors:
Communities: CSHL labs > Lowe lab
Depositing User: Leigh Johnson
Date: 1 August 1998
Date Deposited: 26 Mar 2012 18:10
Last Modified: 26 Mar 2012 18:10
URI: https://repository.cshl.edu/id/eprint/25208

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