ArticleMolecular and cellular biochemistry2002
Different effects of p58PITSLRE on the apoptosis induced by etoposide, cycloheximide and serum-withdrawal in human hepatocarcinoma cells.
Article in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- LPS-stimulating astrocyte-conditioned medium causes neuronal apoptosis via increasing CDK11(p58) expression in PC12 cells through downregulating AKT pathway.Cellular and molecular neurobiology · 2013Article
- Thr-370 is responsible for CDK11(p58) autophosphorylation, dimerization, and kinase activity.The Journal of biological chemistry · 2011Article
- CDK11(p58) protein kinase activity is associated with Bcl-2 down-regulation in pro-apoptosis pathway.Molecular and cellular biochemistry · 2007Article
- Involvement of beta 1,4 galactosyltransferase 1 and Gal beta1-->4GlcNAc groups in human hepatocarcinoma cell apoptosis.Molecular and cellular biochemistry · 2003Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Minimal overexpression of the p58PITSLRE protein kinase in Chinese hamster ovary cells induces telephase delay, abnormal cytokinesis, retarded cell growth and apoptosis. Fas mediated T cell death is correlated with p58PITSLRE proteolysis and an increase in its histone H1 kinase activity. In this study, it was found that p58PITSLRE had different effects on the apoptosis induced by etoposide, cycloheximide and serum-withdrawal in human hepatocarcinoma cells. The ectopic expression of p58PITSLRE in human hepatocarcinoma cells suppressed apoptosis induced by etoposide, while enhancing the apoptosis induced by cycloheximide and serum-withdrawal respectively. Elevated expression of p58PITSLRE was found during the apoptosis induced by etoposide, whereas most of p58PITSLRE was proteolytically processed during apoptosis induced by cycloheximide and serum-withdrawal. Furthermore, transient transfection of p50PITSLRE resembling the proteolytic form of p58PITSLRE enhanced the 7,721 cells susceptibility to apoptosis induced by all the three stimuli. These findings suggest that the full-length p58PITSLRE might protect the cells from the apoptosis induced by etoposide and its proteolysis might contribute to and enhance the apoptosis induced by cycloheximide and serum-withdrawal respectively.
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