| Arrest of the cell cycle reduces susceptibility of target cells to perforin-mediated lysis. | |
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MedLine Citation:
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PMID: 9620169 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cytotoxic T lymphocytes secrete a pore-forming cytolysin, perforin, that damages membranes of target cells. They also ligate Fas receptors on target cells and provoke apoptotic death. A20 (B lymphoma) and P815 (mastocytoma) cell lines were examined for their susceptibility to perforin-mediated lysis and to Fas-induced apoptosis after blockade of the cell cycle at the G1/S interface. Cells were arrested at the G1/S interface by inhibition of DNA synthesis with thymidine or aphidicolin. Subsequently, the treated cells were incubated either with CTL cytotoxic granules or the Fas-specific monoclonal antibody Jo-2. We show that arrest of the cell cycle at the G1/S interface markedly reduced the susceptibility of target cells to perforin-mediated lysis. In contrast, growth arrest with thymidine or aphidicolin increased susceptibility of A20 and P815 cells to Fas-mediated apoptosis. Susceptibility to lysis by intact CTLs was not affected significantly by blockade of target cells with aphidicolin or thymidine. When cells surviving exposure to perforin-containing granules were isolated on Ficoll density gradients and cell-cycle profiles were examined by flow cytometry, the ratio of G1 to G2 cells increased among the survivors exposed to granules in contrast to controls incubated with buffer alone. The data suggest that cells in G1 phase of the cell cycle are less susceptible to the perforin pathway than cells in G2 and S phases but are more susceptible to the Fas pathway. |
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Authors:
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M De Leon; K M Jackson; J R Cavanaugh; D Mbangkollo; C R Verret |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cellular biochemistry Volume: 69 ISSN: 0730-2312 ISO Abbreviation: J. Cell. Biochem. Publication Date: 1998 Jun |
Date Detail:
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Created Date: 1998-07-23 Completed Date: 1998-07-23 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8205768 Medline TA: J Cell Biochem Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 425-35 Citation Subset: IM |
Affiliation:
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Department of Chemistry, Clark Atlanta University, Atlanta, Georgia 30314, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD95 / physiology Aphidicolin / pharmacology Apoptosis / immunology* Cell Cycle / immunology* Cell Death Cell Line Cytoplasmic Granules Cytotoxicity, Immunologic Lymphoma, B-Cell Mast-Cell Sarcoma Membrane Glycoproteins / pharmacology* Mice Perforin Pore Forming Cytotoxic Proteins T-Lymphocytes, Cytotoxic / immunology* Thymidine / pharmacology Tumor Cells, Cultured |
| Grant Support | |
ID/Acronym/Agency:
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G12RR03062/RR/NCRR NIH HHS; S06GM08247/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD95; 0/Membrane Glycoproteins; 0/Pore Forming Cytotoxic Proteins; 126465-35-8/Perforin; 38966-21-1/Aphidicolin; 50-89-5/Thymidine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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