Critical Reviews™ in Eukaryotic Gene Expression

ISSN for PRINT: 1045-4403

For Online Access

Best Paper Award Selection - Editorial Board Site

2000, Volume10

Issue 3&4

124 pages

Issue price - $338.00

David G. Breckenridge
Department of Biochemistry, Mclntyre Medical Sciences Building, McGill University, Montreal, Quebec, Canada H3G 1Y6

Gordon C. Shore
Department of Biochemistry, Mclntyre Medical Sciences Building, McGill University, Montreal, Quebec, Canada H3G 1Y6

E1A and c-myc are oncogenes that can deregulate the cell cycle and promote transformation under conditions where normal cell-cycle checkpoints are inactivated. In situations where cell-cycle checkpoints are intact, the E1A and c-Myc proteins potently induce apoptosis, a property that is believed to be the end result of a cellular response to uncontrolled growth-promoting signals. p53 is a key regulator of E1A and c-myc-induced apoptosis and, together with the oncoproteins, may transcriptionally activate numerous genes whose products influence, or are themselves, members of the core apoptotic machinery. The upstream signaling events and the ultimate apoptotic pathways activated by E1A and c-Myc are discussed in this review.

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