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Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents

Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, dep...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119402/
https://www.ncbi.nlm.nih.gov/pubmed/1402650
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description Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, deprived of IL-3. In contrast, when cultured in the presence of IL-3, or other growth promoting factors, BAF3 cells are highly resistant to X-irradiation and the cytotoxic drugs etoposide and cisplatin. Overexpression of the bcl2 gene product also protects BAF3 cells from DNA damage. The presence of IL-3 is not required during the initial events of DNA damage or its repair. In the absence of IL-3, cells still complete the repair of DNA breaks within 15 min, and continue to cycle for 5 h. At this time, IL-3 is necessary to prevent the accelerated onset of DNA cleavage from a G2 arrest point.
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spelling pubmed-21194022008-04-16 Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents J Exp Med Articles Murine bone marrow-derived cells, dependent on interleukin 3 (IL-3) for their growth in culture, undergo programmed cell, or apoptosis, upon cytokine withdrawal. Here it is reported that a variety of DNA damaging agents cause a more rapid onset of apoptosis in a factor-dependent cell line, BAF3, deprived of IL-3. In contrast, when cultured in the presence of IL-3, or other growth promoting factors, BAF3 cells are highly resistant to X-irradiation and the cytotoxic drugs etoposide and cisplatin. Overexpression of the bcl2 gene product also protects BAF3 cells from DNA damage. The presence of IL-3 is not required during the initial events of DNA damage or its repair. In the absence of IL-3, cells still complete the repair of DNA breaks within 15 min, and continue to cycle for 5 h. At this time, IL-3 is necessary to prevent the accelerated onset of DNA cleavage from a G2 arrest point. The Rockefeller University Press 1992-10-01 /pmc/articles/PMC2119402/ /pubmed/1402650 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title_full Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title_fullStr Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title_full_unstemmed Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title_short Interleukin 3 protects murine bone marrow cells from apoptosis induced by DNA damaging agents
title_sort interleukin 3 protects murine bone marrow cells from apoptosis induced by dna damaging agents
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119402/
https://www.ncbi.nlm.nih.gov/pubmed/1402650