| 15629159 |
Li Z, Wang H, Zong H, Sun Q, Kong X, Jiang J, Gu J: Downregulation of beta1,4-galactosyltransferase 1 inhibits CDK11 (p58)-mediated apoptosis induced by cycloheximide. Biochem Biophys Res Commun. 2005 Feb 11;327(2):628-36.
Cyclin-dependent kinase 11 (CDK11; also named PITSLRE) is part of the large family of p34 (cdc2)-related kinases whose functions appear to be linked with cell cycle progression, tumorigenesis, and apoptotic signaling. The mechanism that CDK11 (p58) induces apoptosis is not clear. Some evidences suggested beta1,4-galactosyltransferase 1 (beta1,4-GT 1) might participate in apoptosis induced by CDK11 (p58). In this study, we demonstrated that ectopically expressed beta1,4-GT 1 increased CDK11 (p58)-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of beta1,4-GT 1 effectively inhibited apoptosis induced by CHX in CDK11 (p58)-overexpressing cells. For example, the cell morphological and nuclear changes were reduced; the loss of cell viability was prevented and the number of cells in sub-G1 phase was decreased. Knock down of beta1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. Therefore, the cleavage of CDK11 (p58) by caspase-3 was reduced. We proposed that beta1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11 (p58). This may represent a new mechanism of beta1,4-GT 1 in CHX-induced apoptosis of CDK11 (p58)-overexpressing cells. |
87(1,1,1,7) |