First Author | Dansen TB | Year | 2006 |
Journal | J Biol Chem | Volume | 281 |
Issue | 16 | Pages | 10890-5 |
PubMed ID | 16464852 | Mgi Jnum | J:108676 |
Mgi Id | MGI:3624498 | Doi | 10.1074/jbc.M513655200 |
Citation | Dansen TB, et al. (2006) Specific requirement for Bax, not Bak, in Myc-induced apoptosis and tumor suppression in vivo. J Biol Chem 281(16):10890-5 |
abstractText | 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. |