A novel splice variant of the cell death-promoting protein BAX.
Cell death plays an important role in a number of physiological processes in all complex multicellular organisms. One of the molecules that regulates this process is BAX, an integral membrane protein, that promotes apoptosis. The function of BAX is countered by BCL-2 and BCL-XL. The differential expression of these proteins can influence the ability of the cell to die or survive. In this paper, we describe the cloning, biochemical, and functional characterization of a novel splice isoform of BAX, called BAX-omega. Transient overexpression of BAX-omega protein potentiates cell death at levels comparable to that of BAX-alpha overexpression.
Zhou
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Department of Cell Biology, Neurex Corporation, Menlo Park, California 94025, USA.
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McClure
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Crea
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Bitler
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D017398:Alternative Splicing; D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis; D019556:COS Cells; D003001:Cloning, Molecular; D006801:Humans; D008969:Molecular Sequence Data; D016716:PC12 Cells; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D014018:Tissue Distribution; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; C494828:Bax protein, rat; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein