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pubmed-article:9770349pubmed:abstractTextFGF-1 stimulated DNA synthesis and induced expression of IL-2 receptors in the murine fibrosarcoma cell line, F69-3. Concomitant treatment with IL-2 abolished the stimulation of DNA synthesis, but not binding of FGF-1 to the FGF-receptors or subsequent endocytosis of the bound growth factor. Also, it did not inhibit activation of the FGF-receptor tyrosine kinase or stimulation of the downstream effector, MAP kinase. Treatment with IL-2 prevented transport of FGF-1 to the nuclear fraction in a time- and dose-dependent manner that parallelled the inhibition of FGF-1 stimulated DNA synthesis. The data support our earlier finding that transport of FGF-1 to the nucleus is an important event in the mechanism of stimulation of DNA synthesis induced by the growth factor, and they demonstrate that treatment with a cytokine can modulate the cellular response to FGF-1.lld:pubmed
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pubmed-article:9770349pubmed:copyrightInfoCopyright 1998 Academic Press.lld:pubmed
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pubmed-article:9770349pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:9770349pubmed:articleTitleModulation by interleukin-2 of cellular response to fibroblast growth factor-1 in F69-3 fibrosarcoma cells.lld:pubmed
pubmed-article:9770349pubmed:affiliationInstitute for Cancer Research, The Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway.lld:pubmed
pubmed-article:9770349pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9770349pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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