Bcl-2 and Bax function independently to regulate cell death.
The BCL-2 family has various pairs of antagonist and agonist proteins that regulate apoptosis. Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between Bax and Bcl-2, each is able to regulate apoptosis independently.
Knudson
C M
CM
Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Korsmeyer
S J
SJ
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002453:Cell Cycle; D006224:Cricetinae; D017353:Gene Deletion; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000502:physiology*; D011817:Rabbits; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; C494827:Bax protein, mouse; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein