BCL-2 AND BAX FUNCTION INDEPENDENTLY TO REGULATE CELL-DEATH

Citation
Cm. Knudson et Sj. Korsmeyer, BCL-2 AND BAX FUNCTION INDEPENDENTLY TO REGULATE CELL-DEATH, Nature genetics, 16(4), 1997, pp. 358-363
Citations number
40
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
10614036
Volume
16
Issue
4
Year of publication
1997
Pages
358 - 363
Database
ISI
SICI code
1061-4036(1997)16:4<358:BABFIT>2.0.ZU;2-P
Abstract
The BCL-2 family has Various pairs of antagonist and agonist proteins that regulate apoptosis, Whether their function is interdependent is u ncertain. Using a genetic approach to address this question, we utiliz ed gain- and loss-of-function models of Bcl-2 and Bar and found that a poptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice are largely absent in mice also deficient in Bax. A single copy of Bar promoted apoptosis in the absence of Bcl-2. In contrast, overexpressi on of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between Bar and Bcl-2, each is able to regu late apoptosis independently.