Abstract
Cyclin-dependent kinase 11 (CDK11; also named PITSLRE) is part of the large family of p34{sup cdc2}-related kinases whose functions appear to be linked with cell cycle progression, tumorigenesis, and apoptotic signaling. The mechanism that CDK11{sup p58} induces apoptosis is not clear. Some evidences suggested {beta}1,4-galactosyltransferase 1 ({beta}1,4-GT 1) might participate in apoptosis induced by CDK11{sup p58}. In this study, we demonstrated that ectopically expressed {beta}1,4-GT 1 increased CDK11{sup p58}-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of {beta}1,4-GT 1 effectively inhibited apoptosis induced by CHX in CDK11{sup 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 {beta}1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. Therefore, the cleavage of CDK11{sup p58} by caspase-3 was reduced. We proposed that {beta}1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11{sup p58}. This may represent a new mechanism of {beta}1,4-GT 1 in CHX-induced apoptosis of CDK11{sup p58}-overexpressing cells.
Zejuan, Li;
[1]
Hanzhou, Wang;
[1]
Hongliang, Zong;
[1]
Qing, Sun;
[1]
Xiangfei, Kong;
[1]
Jianhai, Jiang;
[1]
Jianxin, Gu
[1]
- State Key Laboratory of Genetic Engineering and Gene Research Center, Shanghai Medical College of Fudan University, Box 103, Shanghai 200032 (China)
Citation Formats
Zejuan, Li, Hanzhou, Wang, Hongliang, Zong, Qing, Sun, Xiangfei, Kong, Jianhai, Jiang, and Jianxin, Gu.
Downregulation of {beta}1,4-galactosyltransferase 1 inhibits CDK11{sup p58}-mediated apoptosis induced by cycloheximide.
United States: N. p.,
2005.
Web.
doi:10.1016/j.bbrc.2004.12.047.
Zejuan, Li, Hanzhou, Wang, Hongliang, Zong, Qing, Sun, Xiangfei, Kong, Jianhai, Jiang, & Jianxin, Gu.
Downregulation of {beta}1,4-galactosyltransferase 1 inhibits CDK11{sup p58}-mediated apoptosis induced by cycloheximide.
United States.
https://doi.org/10.1016/j.bbrc.2004.12.047
Zejuan, Li, Hanzhou, Wang, Hongliang, Zong, Qing, Sun, Xiangfei, Kong, Jianhai, Jiang, and Jianxin, Gu.
2005.
"Downregulation of {beta}1,4-galactosyltransferase 1 inhibits CDK11{sup p58}-mediated apoptosis induced by cycloheximide."
United States.
https://doi.org/10.1016/j.bbrc.2004.12.047.
@misc{etde_20619385,
title = {Downregulation of {beta}1,4-galactosyltransferase 1 inhibits CDK11{sup p58}-mediated apoptosis induced by cycloheximide}
author = {Zejuan, Li, Hanzhou, Wang, Hongliang, Zong, Qing, Sun, Xiangfei, Kong, Jianhai, Jiang, and Jianxin, Gu}
abstractNote = {Cyclin-dependent kinase 11 (CDK11; also named PITSLRE) is part of the large family of p34{sup cdc2}-related kinases whose functions appear to be linked with cell cycle progression, tumorigenesis, and apoptotic signaling. The mechanism that CDK11{sup p58} induces apoptosis is not clear. Some evidences suggested {beta}1,4-galactosyltransferase 1 ({beta}1,4-GT 1) might participate in apoptosis induced by CDK11{sup p58}. In this study, we demonstrated that ectopically expressed {beta}1,4-GT 1 increased CDK11{sup p58}-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of {beta}1,4-GT 1 effectively inhibited apoptosis induced by CHX in CDK11{sup 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 {beta}1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. Therefore, the cleavage of CDK11{sup p58} by caspase-3 was reduced. We proposed that {beta}1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11{sup p58}. This may represent a new mechanism of {beta}1,4-GT 1 in CHX-induced apoptosis of CDK11{sup p58}-overexpressing cells.}
doi = {10.1016/j.bbrc.2004.12.047}
journal = []
issue = {2}
volume = {327}
journal type = {AC}
place = {United States}
year = {2005}
month = {Feb}
}
title = {Downregulation of {beta}1,4-galactosyltransferase 1 inhibits CDK11{sup p58}-mediated apoptosis induced by cycloheximide}
author = {Zejuan, Li, Hanzhou, Wang, Hongliang, Zong, Qing, Sun, Xiangfei, Kong, Jianhai, Jiang, and Jianxin, Gu}
abstractNote = {Cyclin-dependent kinase 11 (CDK11; also named PITSLRE) is part of the large family of p34{sup cdc2}-related kinases whose functions appear to be linked with cell cycle progression, tumorigenesis, and apoptotic signaling. The mechanism that CDK11{sup p58} induces apoptosis is not clear. Some evidences suggested {beta}1,4-galactosyltransferase 1 ({beta}1,4-GT 1) might participate in apoptosis induced by CDK11{sup p58}. In this study, we demonstrated that ectopically expressed {beta}1,4-GT 1 increased CDK11{sup p58}-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of {beta}1,4-GT 1 effectively inhibited apoptosis induced by CHX in CDK11{sup 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 {beta}1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. Therefore, the cleavage of CDK11{sup p58} by caspase-3 was reduced. We proposed that {beta}1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11{sup p58}. This may represent a new mechanism of {beta}1,4-GT 1 in CHX-induced apoptosis of CDK11{sup p58}-overexpressing cells.}
doi = {10.1016/j.bbrc.2004.12.047}
journal = []
issue = {2}
volume = {327}
journal type = {AC}
place = {United States}
year = {2005}
month = {Feb}
}