Bax Can Antagonize Bcl-XL during Etoposide and Cisplatin-induced Cell Death Independently of Its Heterodimerization with Bcl-XL
Authors:
- Didier A. M. GrillotDGDidier A. M. Grillot
- Ramón MerinoRMRamón Merino
- Gabriel Nu~EzGNGabriel Nu~Ez
Open Access
- 1 September 1996
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 271 (37) , 22764-22772
Abstract
No abstract availableKeywords
This publication has 25 references indexed in Scilit:
- The E1B 19K protein blocks apoptosis by interacting with and inhibiting the p53-inducible and death-promoting Bax protein.Genes & Development, 1996
- Bax-independent inhibition of apoptosis by Bcl-XLNature, 1996
- Life, death, and the pursuit of apoptosis.Genes & Development, 1996
- CD28 costimulation can promote T cell survival by enhancing the expression of Bcl-xLImmunity, 1995
- Apoptosis in the Pathogenesis and Treatment of DiseaseScience, 1995
- Checkpoints of dueling dimers foil death wishesCell, 1994
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993
- bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell deathCell, 1993
- Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cellsNature, 1988
- The t(14;18) Chromosome Translocations Involved in B-Cell Neoplasms Result from Mistakes in VDJ JoiningScience, 1985