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- Title
Bcl-x<sub>L</sub>/Bcl-2 coordinately regulates apoptosis, cell cycle arrest and cell cycle entry.
- Authors
Y.M. Janumyan; C.G. Sansam; A. Chattopadhyay; N. Cheng; E.L. Soucie; L.Z. Penn; D. Andrews; C.M. Knudson; E. Yang
- Abstract
Bcl-xL and Bcl-2 inhibit both apoptosis and proliferation. In investigating the relationship between these two functions of Bcl-xL and Bcl-2, an analysis of 24 Bcl-xL and Bcl-2 mutant alleles, including substitutions at residue Y28 previously reported to selectively abolish the cell cycle activity, showed that cell cycle delay and anti-apoptosis co-segregated in all cases. In determining whether Bcl-2 and Bcl-xL act in G0 or G1, forward scatter and pyronin Y fluorescence measurements indicated that Bcl-2 and Bcl-xL cells arrested more effectively in G0 than controls, and were delayed in G0-G1 transition. The cell cycle effects of Bcl-2 and Bcl-xL were reversed by Bad, a molecule that counters the survival function of Bcl-2 and Bcl-xL. When control and Bcl-xL cells of equivalent size and pyronin Y fluorescence were compared, the kinetics of cell cycle entry were similar, demonstrating that the ability of Bcl-xL and Bcl-2 cells to enhance G0 arrest contributes significantly to cell cycle delay. Our data suggest that cell cycle effects and increased survival both result from intrinsic functions of Bcl-2 and Bcl-xL.
- Publication
EMBO Journal, 2003, Vol 22, Issue 20, p5459
- ISSN
0261-4189
- Publication type
Academic Journal
- DOI
10.1093/emboj/cdg533