Specific requirement for Bax, not Bak, in Myc-induced apoptosis and tumor suppression in vivo |
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Authors: | Dansen Tobias B Whitfield Jonathan Rostker Fanya Brown-Swigart Lamorna Evan Gerard I |
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Affiliation: | Cancer Research Institute and Department of Cellular and Molecular Pharmacology, Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94143-0875, USA. |
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Abstract: | Bax and Bak comprise the mitochondrial gateway for apoptosis induced by diverse stimuli. Loss of both bax and bak is necessary to block cell death induced by such stimuli, indicating a great degree of functional overlap between Bax and Bak. Apoptosis is the major intrinsic pathway that limits the oncogenic potential of Myc. Using a switchable mouse model of Myc-induced apoptosis in pancreatic beta cells, we have shown that Myc induces apoptosis in vivo exclusively through Bax but not Bak. Furthermore, blockade of Myc-induced apoptosis by the inactivation of Bax, but not Bak, eliminates all restraints to the oncogenic potential of Myc, allowing the rapid and synchronous progression of invasive, angiogenic tumors. |
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