CU Molecular, Cellular, and Developmental Biology
MCDB Home > Postdoctoral > PostDocPublications > BreckenridgeDGPublications > Regulation of apoptosis by E1A and Myc oncoproteins
Document Actions

Regulation of apoptosis by E1A and Myc oncoproteins


Regulation of apoptosis by E1A and Myc oncoproteins

5394

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.


Breckenridge DG, Shore GC

Critical reviews in eukaryotic gene expression

2000-01-01 00:00

10

3

273-80

Adenovirus E1A Proteins,Apoptosis,Humans,Proto-Oncogene Proteins c-myc,Signal Transduction,Tumor Suppressor Protein p53,Adenovirus E1A Proteins,Proto-Oncogene Proteins c-myc,Tumor Suppressor Protein p53

Department of Biochemistry, McGill University, Montreal, Quebec, Canada.

Crit. Rev. Eukaryot. Gene Expr.


1045-4403




0

False

11272469

David Breckenridge
University of Colorado Contact Us  |   Legal & Trademarks  |  Privacy