Downregulation of β1,4-galactosyltransferase 1 inhibits CDK11 p58-mediated apoptosis induced by cycloheximide

Zejuan Li, Hanzhou Wang, Hongliang Zong, Qing Sun, Xiangfei Kong, Jianhai Jiang, Jianxin Gu

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


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 β1,4-galactosyltransferase 1 (β1,4-GT 1) might participate in apoptosis induced by CDK11 p58. In this study, we demonstrated that ectopically expressed β1,4-GT 1 increased CDK11 p58-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of β1,4-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 β1,4-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 β1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11 p58. This may represent a new mechanism of β1,4-GT 1 in CHX-induced apoptosis of CDK11 p58-overexpressing cells.

Original languageEnglish (US)
Pages (from-to)628-636
Number of pages9
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Feb 11 2005


  • Apoptosis
  • CDK11
  • CHX
  • SMMC-7721 cells
  • β1,4-GT 1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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