Abstract:
:CDK11(p58), a G2/M-specific protein kinase, has been shown to be associated with apoptosis in many cell lines, with largely unknown mechanisms. Our previous study proved that CDK11(p58)-enhanced cycloheximide (CHX)-induced apoptosis in SMMC-7721 hepatocarcinoma cells. Here we report for the first time that ectopic expression of CDK11(p58) down-regulates Bcl-2 expression and its Ser70, Ser87 phosphorylation in CHX-induced apoptosis in SMMC-7721 cells. Overexpression of Bcl-2 counteracts the pro-apoptotic activity of CDK11(p58). Furthermore, we confirm that the kinase activity of CDK11(p58) is essential to the down-regulation of Bcl-2 as well as apoptosis. Taken together, these results demonstrate that CDK11(p58) down-regulates Bcl-2 in pro-apoptosis pathway depending on its kinase activity, which elicits survival signal in hepatocarcinoma cells.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Yun X,Wu Y,Yao L,Zong H,Hong Y,Jiang J,Yang J,Zhang Z,Gu Jdoi
10.1007/s11010-007-9502-xsubject
Has Abstractpub_date
2007-10-01 00:00:00pages
213-8issue
1-2eissn
0300-8177issn
1573-4919journal_volume
304pub_type
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