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Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line

In the absence of a survival stimulus, the interleukin 3 (IL-3)- dependent IC.DP cell line undergoes a process termed programmed cell death or apoptosis. Survival can be induced by IL-3, which can also stimulate proliferation of IC.DP cells. IC.DP cells have been stably transfected with the p160v-ab...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1994
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191668/
https://www.ncbi.nlm.nih.gov/pubmed/8064240
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collection PubMed
description In the absence of a survival stimulus, the interleukin 3 (IL-3)- dependent IC.DP cell line undergoes a process termed programmed cell death or apoptosis. Survival can be induced by IL-3, which can also stimulate proliferation of IC.DP cells. IC.DP cells have been stably transfected with the p160v-abl protein tyrosine kinase, activation of the kinase at the permissive temperature permits cell survival in the absence of IL-3 by suppression of apoptosis, although the growth factor is still required for proliferation. Both IL-3 and activation of the v- ABL tyrosine kinase stimulated glucose transport, which may in part be due to a translocation of transporters to the cell surface. Inhibition of glucose uptake markedly increased the rate of apoptosis in these cells, an effect that could be reversed by the provision of alternative energy sources such as glutamine. Growth factor- or oncogene-mediated increases in glucose uptake may therefore represent an important regulatory point in the suppression of apoptosis.
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spelling pubmed-21916682008-04-16 Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line J Exp Med Articles In the absence of a survival stimulus, the interleukin 3 (IL-3)- dependent IC.DP cell line undergoes a process termed programmed cell death or apoptosis. Survival can be induced by IL-3, which can also stimulate proliferation of IC.DP cells. IC.DP cells have been stably transfected with the p160v-abl protein tyrosine kinase, activation of the kinase at the permissive temperature permits cell survival in the absence of IL-3 by suppression of apoptosis, although the growth factor is still required for proliferation. Both IL-3 and activation of the v- ABL tyrosine kinase stimulated glucose transport, which may in part be due to a translocation of transporters to the cell surface. Inhibition of glucose uptake markedly increased the rate of apoptosis in these cells, an effect that could be reversed by the provision of alternative energy sources such as glutamine. Growth factor- or oncogene-mediated increases in glucose uptake may therefore represent an important regulatory point in the suppression of apoptosis. The Rockefeller University Press 1994-09-01 /pmc/articles/PMC2191668/ /pubmed/8064240 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
Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title_full Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title_fullStr Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title_full_unstemmed Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title_short Apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
title_sort apoptosis is regulated by the rate of glucose transport in an interleukin 3 dependent cell line
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191668/
https://www.ncbi.nlm.nih.gov/pubmed/8064240