PMID: 8600029Feb 15, 1996Paper

The E1B 19K protein blocks apoptosis by interacting with and inhibiting the p53-inducible and death-promoting Bax protein

Genes & Development
J HanE White

Abstract

The E1B 19K protein is a potent apoptosis inhibitor and the putative adenovirus Bcl-2 homolog. To investigate the mechanism of apoptosis regulation, 19K-interacting cellular proteins were identified using the yeast two-hybrid system, and Bax was one of seven 19-K interacting clones. Residues 50-78 of Bax containing a conserved region designated Bcl-2 homology region 3 (BH3) were sufficient for specific binding to both the E1B 19K and Bcl-2 proteins. The Bax-E1B 19K interaction was detectable in vitro and in lysates from mammalian cells, and Bax expression antagonized E1B 19K protein function. bax mRNA and protein levels were p53-inducible with kinetics identical to that of p21/Waf-1/Cip-1, and E1B 19K and Bcl-2 expression did not affect Bax or p21/Waf-1/Cip-1 accumulation. In cells where p53 was mutant, Bax expression induced apoptosis, suggesting that Bax was sufficient for apoptosis, and acted downstream of p53. p53 may simultaneously activate the transcription of genes required for both growth arrest (p21/Waf-1/Cip-1) and death (bax), and E1B 19K and Bcl-2 may act distally and function through interaction with and antagonism of Bax to prevent apoptosis. With the death pathway disabled, induction of growth arrest by p53 can t...Continue Reading

References

Aug 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·S J KuerbitzM B Kastan
Nov 1, 1992·The Journal of Cell Biology·Y GavrieliS A Ben-Sasson
Aug 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·L RaoE White
Apr 3, 1992·Cell·G I EvanD C Hancock
Jul 5, 1991·Science·M HollsteinC C Harris
Dec 20, 1990·Nature·B Vogelstein
Dec 1, 1989·Proceedings of the National Academy of Sciences of the United States of America·E White, R Cipriani
Sep 1, 1995·Genes & Development·Y HauptM Oren
Sep 1, 1995·Genes & Development·P SabbatiniE White
Mar 1, 1995·Genes & Development·C E CanmanM B Kastan
Apr 20, 1995·Nature·T ChittendenB C Guild
Sep 27, 1994·Proceedings of the National Academy of Sciences of the United States of America·T SatoH G Wang
Sep 30, 1994·Science·H Hermeking, D Eick
Mar 15, 1994·Proceedings of the National Academy of Sciences of the United States of America·S W LoweH E Ruley
Apr 1, 1994·Molecular and Cellular Biology·S K ChiouE White
Nov 19, 1993·Cell·W S el-DeiryB Vogelstein
Dec 16, 1993·Nature·Y XiongD Beach
Apr 1, 1993·Genes & Development·M Debbas, E White
Sep 15, 1993·Proceedings of the National Academy of Sciences of the United States of America·S HendersonA Rickinson
Feb 1, 1993·Current Opinion in Genetics & Development·E Moran

❮ Previous
Next ❯

Citations

May 29, 1997·International Journal of Cancer. Journal International Du Cancer·S TheisK Roemer
Jul 29, 1998·International Journal of Cancer. Journal International Du Cancer·U Naumann, M Weller
Jan 24, 1998·Journal of Cellular Biochemistry·G Condorelli, A Giordano
Aug 1, 1997·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·A Metcalfe, C Streuli
Sep 26, 2002·Virus Research·Adrienne L McNees, Linda R Gooding
Aug 21, 2003·Toxicology Letters·Yoshiko YokoyamaKazutaka Kano
Dec 6, 1997·Current Opinion in Genetics & Development·J L Rinkenberger, S J Korsmeyer
Feb 1, 1997·Current Opinion in Genetics & Development·L Rao, E White
Aug 15, 1998·Trends in Cell Biology·A Kelekar, C B Thompson
Mar 1, 1997·Trends in Microbiology·J C NeilE W Baxter
Apr 20, 2001·Critical Reviews in Oncology/hematology·H H Sedlacek
Dec 1, 1996·Immunology and Cell Biology·S Cuff, J Ruby
Dec 4, 2009·The Journal of Biological Chemistry·Stephanie CampbellMichele Barry
Dec 31, 2010·The Journal of Biological Chemistry·Marcin StawowczykNancy C Reich
Dec 1, 1996·The Journal of Cell Biology·L RaoE White
Apr 3, 2002·The Journal of Experimental Medicine·Marcia A Blackman, Emilio Flaño
Jun 14, 2003·Journal of Neurotrauma·Ramesh RaghupathiTracy K McIntosh
May 15, 2004·DNA and Cell Biology·Shohreh AminiBassel E Sawaya
Nov 25, 2003·Genes & Development·Andrea CuconatiEileen White
Jul 10, 1999·Immunological Reviews·J A Mahr, L R Gooding
Jul 1, 2004·Science's STKE : Signal Transduction Knowledge Environment·John C ReedAdam Godzik
Jul 20, 2001·Journal of Virology·R Sundararajan, E White
Oct 22, 2002·Journal of Virology·Elena LomonosovaG Chinnadurai
Jan 19, 2002·Journal of Virology·Alexander R MoiseWilfred A Jefferies
Aug 9, 2002·Molecular and Cellular Biology·Philippe JuinGerard Evan
Jan 1, 1997·Annual Review of Microbiology·D E Griffin, J M Hardwick
Jun 3, 2008·PLoS Pathogens·Lorenzo GalluzziGuido Kroemer

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis