| Mechanism of apoptosis suppression by phorbol ester in IL-6-starved murine plasmacytomas: role of PKC modulation and cell cycle. | |
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MedLine Citation:
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PMID: 8703964 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We show here that the mode of cell death in IL-6-starved T1165 and T1198 plasmacytoma cell lines is apoptosis, and that it can be suppressed by phorbol ester (PMA) treatment in a protein kinase C (PKC)-mediated process that involves alpha and/or delta isozymes. PMA-induced PKC activation, but not the depletion that follows it, participates in the suppression of apoptosis. Extended PKC activation is necessary but not sufficient for the apoptosis suppression. In addition, the cells must be in a "competent" state, which appears not to be determined by PKC. We observed two points of "competence" during the time between withdrawal of IL-6 and the start of massive cell death: one, immediately after withdrawal, and another, just before onset of apoptosis, at the time corresponding to maximal accumulation of cells in a G0/G1 block imposed by IL-6 withdrawal. Treatment with PMA and other PKC activators resulted in a shift of the cell population to S phase, lifting the G0/G1 block. We propose a model in which cells are rescued in a certain stage of the G1 phase of cell cycle. Death suppression occurs when a transient PMA-induced PKC activation occurs when a significant number of cells are in this part of G1, allowing them to pass the restriction point safely without initiating the cell death program. |
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Authors:
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L Y Romanova; I A Alexandrov; G Schwab; D M Hilbert; J F Mushinski; R P Nordan |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Biochemistry Volume: 35 ISSN: 0006-2960 ISO Abbreviation: Biochemistry Publication Date: 1996 Jul |
Date Detail:
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Created Date: 1996-09-10 Completed Date: 1996-09-10 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0370623 Medline TA: Biochemistry Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 9900-6 Citation Subset: IM |
Affiliation:
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Laboratory of Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alkaloids Animals Apoptosis / drug effects* Benzophenanthridines Cell Cycle* / drug effects Cell Line Cytosol / enzymology Enzyme Activation Enzyme Inhibitors / pharmacology Indoles / pharmacology Interleukin-6 / pharmacology* Isoenzymes / antagonists & inhibitors, metabolism Lactams / pharmacology Maleimides / pharmacology Mice Phenanthridines / pharmacology Phorbol Esters / pharmacology Plasmacytoma Protein Kinase C / antagonists & inhibitors, metabolism* Tetradecanoylphorbol Acetate / analogs & derivatives, pharmacology* Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Alkaloids; 0/Benzophenanthridines; 0/Enzyme Inhibitors; 0/Indoles; 0/Interleukin-6; 0/Isoenzymes; 0/Lactams; 0/Maleimides; 0/Phenanthridines; 0/Phorbol Esters; 109346-66-9/7-octylindolactam V; 133052-90-1/bisindolylmaleimide I; 16561-29-8/Tetradecanoylphorbol Acetate; 34316-15-9/chelerythrine; 94482-56-1/thymeleatoxin; EC 2.7.11.13/Protein Kinase C |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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