Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death
- 1 January 1995
- Vol. 80 (2) , 285-291
- https://doi.org/10.1016/0092-8674(95)90411-5
Abstract
No abstract availableKeywords
This publication has 20 references indexed in Scilit:
- 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
- Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activityCell, 1993
- Oncogenic activity of the c-Myc protein requires dimerization with MaxCell, 1993
- Prevention of Programmed Cell Death in Caenorhabditis elegans by Human bcl-2Science, 1992
- Ultrastructural localization of bcl-2 protein.Journal of Histochemistry & Cytochemistry, 1992
- Prevention of Programmed Cell Death of Sympathetic Neurons by the bcl-2 Proto-OncogeneScience, 1992
- Interaction Cloning: Identification of a Helix-Loop-Helix Zipper Protein that Interacts with c-FosScience, 1992
- Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell deathNature, 1990
- Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cellsNature, 1988