The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteins

Rao, L., Debbas, M., Sabbatini, P., Hockenbery, D., Korsmeyer, S., White, E. (August 1992) The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteins. Proceedings of the National Academy of Sciences of the United States of America, 89 (16). pp. 7742-7746. ISSN 0027-8424

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Abstract

Cooperation between the adenovirus E1A and E1B oncogenes is required for transformation of primary quiescent rodent cells. Although expression of E1A alone will stimulate cell proliferation sufficient to initiate transformed focus formation, proliferation fails to be sustained and foci degenerate. Coexpression of either the 19-kDa or 55-kDa E1B oncoproteins with E1A permits high-frequency transformation by overcoming this cytotoxic response. Without E1B 19-kDa protein expression, however, transformants remain susceptible to induction of cell death. Rapid loss of viability is coincident with nucleolytic cleavage of DNA in intranucleosomal regions and chromatin condensation, hallmarks of programed cell death (apoptosis). Furthermore, overexpression of a known suppressor of apoptosis, the Bcl-2 protooncogene, can rescue E1A-induced focus degeneration. Thus E1A-dependent stimulation of cell proliferation is accompanied by apoptosis and thereby insufficient to singly induce transformation. High-frequency transformation requires a second function encoded by the E1B 19-kDa protein to block apoptosis.

Item Type: Paper
Uncontrolled Keywords: TUMOR-NECROSIS-FACTOR PROGRAMMED CELL-DEATH EARLY REGION E1B GENE-EXPRESSION INTERMEDIATE FILAMENTS 19-KILODALTON PROTEIN TRANSFORMED-CELLS FACTOR CYTOLYSIS MOUSE CELLS HOST-CELL
Subjects: organism description > virus > adenovirus
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > oncogene
CSHL Authors:
Communities: CSHL labs
Depositing User: Matt Covey
Date: August 1992
Date Deposited: 22 Sep 2015 19:45
Last Modified: 30 Sep 2019 14:39
PMCID: PMC49787
Related URLs:
URI: https://repository.cshl.edu/id/eprint/31859

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