Display options
Cite
Gottschalk AR, Boise LH, Oltvai ZN, et al. The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated. Cell Death Differ. 1996;3(1):113-8
Gottschalk, A. R., Boise, L. H., Oltvai, Z. N., Accavitti, M. A., Korsmeyer, S. J., Quintáns, J., & Thompson, C. B. (1996). The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated. Cell death and differentiation, 3(1), 113-8.
Gottschalk, A R, et al. "The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated." Cell death and differentiation vol. 3,1 (1996): 113-8.
Gottschalk AR, Boise LH, Oltvai ZN, Accavitti MA, Korsmeyer SJ, Quintáns J, Thompson CB. The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated. Cell Death Differ. 1996 Jan;3(1):113-8. PMID: 17180062.
Copy Download .nbib Format: NLM
Share it on

Cell Death Differ. 1996 Jan;3(1):113-8.

The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated.

Cell death and differentiation

A R Gottschalk, L H Boise, Z N Oltvai, M A Accavitti, S J Korsmeyer, J Quintáns, C B Thompson

Affiliations

  1. Department of Pathology and Cancer Research Center, University of Chicago.

PMID: 17180062

Abstract

Although expression of Bcl-2 has been shown to prevent apoptosis under many circumstances, there are several systems in which Bcl-2 fails to promote cell survival. We have previously reported that Bcl-2 and Bcl-x(L) display differential ability to protect WEHI-231 cells from multiple inducers of apoptosis. A possible explanation for this paradox was provided by the discovery of Bax. Bax is a Bcl-2-related protein which can inhibit the ability of Bcl-2 to enhance the survival of growth factor-dependent cell lines in the absence of growth factor. Consistent with the possibility that Bcl-2 function in WEHI-231 cells is inhibited by Bax, WEHI-231 cells were found to express a high level of Bax. To directly test the effects of Bax expression on Bcl-x(L) function, FL5.12 cells were transfected with both genes. Although Bax overexpression can inhibit Bcl-2 from prolonging cell survival upon growth factor withdrawal, Bax overexpression did not inhibit Bcl-x(L) from preventing apoptosis in this cell line. Although Bcl-2 and Bcl-x(L) were both found to be able to form heterodimers with Bax, the majority of Bax in both cases was not complexed to a partner. Our data suggest that Bcl-x(L) does not function by simply preventing the formation of Bax homodimers which promote cell death. Instead Bax appears to display selectivity in its ability to inhibit Bcl-2 but not Bcl-x(L) from prolonging survival. Furthermore, our data suggest that the abilities of Bcl-2 and Bcl-x(L) to promote cell survival are not identical and can be independently regulated within a cell. Regulation of a cell's apoptotic threshold is likely to result from a complex set of interactions among Bcl-2 family members and other, as yet uncharacterised, regulators of apoptosis.

Publication Types