The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Perillyl alcohol induces c-Myc-dependent apoptosis in Bcr/Abl-transformed leukemia cells.

Bcr/Abl-transformed cells strongly resist apoptosis induced by most chemotherapy agents. However, in Bcr/Abl-transformed cells the monocyclic monoterpene, perillyl alcohol ( POH), induces G0/G1 arrest and apoptosis without affecting Bcr/Abl expression or activity. The primary effect of POH is to cause growth arrest while apoptosis is a consequence of this arrest. Since Bcr/Abl induces constitutive expression of c-Myc, which is necessary for cell cycle transit from G1 into the S phase, we tested whether POH causes growth arrest by inhibiting expression of c-Myc. However, in POH-arrested Bcr/Abl-transformed cells, expression of c-Myc RNA and protein was not affected. Because expression of c-Myc during growth arrest can lead to apoptosis, we examined the role of c-Myc in POH- induced apoptosis. c-Myc induces expression of the ornithine decarboxylase (ODC) gene, which synthesizes polyamines that are necessary for cell growth. Myc- induced apoptosis operates through ODC and can be prevented with the ODC inhibitor, alpha-difluoromethylornithine (DFMO). We report that DFMO strongly protects cells from POH-induced apoptosis. These results show that in Bcr/Abl-transformed cells, POH activates a Myc-ODC apoptotic pathway that is not protected by the Bcr/Abl antiapoptotic mechanism.[1]


WikiGenes - Universities