Proliferative responses and binding properties of hematopoietic cells transfected with low-affinity receptors for leukemia inhibitory factor, oncostatin M, and ciliary neurotrophic factor.
Identifieur interne : 000092 ( Pmc/Curation ); précédent : 000091; suivant : 000093Proliferative responses and binding properties of hematopoietic cells transfected with low-affinity receptors for leukemia inhibitory factor, oncostatin M, and ciliary neurotrophic factor.
Auteurs : D P Gearing ; S F Ziegler ; M R Comeau ; D. Friend ; B. Thoma ; D. Cosman ; L. Park ; B. MosleySource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1994.
Abstract
Specific low-affinity receptors for leukemia inhibitory factor (LIF), oncostatin M (OSM; gp130), and ciliary neurotrophic factor (CNTF; receptor alpha, CNTFR alpha) may be utilized in various combinations to generate high-affinity binding sites and signal transduction. We have tested the ability of combinations of these receptors to transduce a proliferative signal in BAF-B03 cells. Coexpression of the LIF receptor and gp130 in these cells conferred high-affinity LIF and OSM binding and responsiveness to LIF and OSM. These cells also responded to CNTF in the absence of detectable binding. The further addition of CNTFR alpha conferred high-affinity CNTF binding and enhanced responsiveness to CNTF but did not modify responses to LIF or OSM. Coexpression of LIF receptor and CNTFR alpha resulted in a nonfunctional high-affinity binding site. These data are consistent with a role for the CNTFR alpha in enhancing CNTF action but the CNTFR alpha is not absolutely required for CNTF action and suggest a wider range of targets for CNTF.
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PubMed: 8302840
PubMed Central: 521465
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<author><name sortKey="Friend, D" sort="Friend, D" uniqKey="Friend D" first="D" last="Friend">D. Friend</name>
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<author><name sortKey="Thoma, B" sort="Thoma, B" uniqKey="Thoma B" first="B" last="Thoma">B. Thoma</name>
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<series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title>
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<front><div type="abstract" xml:lang="en"><p>Specific low-affinity receptors for leukemia inhibitory factor (LIF), oncostatin M (OSM; gp130), and ciliary neurotrophic factor (CNTF; receptor alpha, CNTFR alpha) may be utilized in various combinations to generate high-affinity binding sites and signal transduction. We have tested the ability of combinations of these receptors to transduce a proliferative signal in BAF-B03 cells. Coexpression of the LIF receptor and gp130 in these cells conferred high-affinity LIF and OSM binding and responsiveness to LIF and OSM. These cells also responded to CNTF in the absence of detectable binding. The further addition of CNTFR alpha conferred high-affinity CNTF binding and enhanced responsiveness to CNTF but did not modify responses to LIF or OSM. Coexpression of LIF receptor and CNTFR alpha resulted in a nonfunctional high-affinity binding site. These data are consistent with a role for the CNTFR alpha in enhancing CNTF action but the CNTFR alpha is not absolutely required for CNTF action and suggest a wider range of targets for CNTF.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id>
<journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title>
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<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
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<title-group><article-title>Proliferative responses and binding properties of hematopoietic cells transfected with low-affinity receptors for leukemia inhibitory factor, oncostatin M, and ciliary neurotrophic factor.</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Gearing</surname>
<given-names>D P</given-names>
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<contrib contrib-type="author"><name><surname>Ziegler</surname>
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<contrib contrib-type="author"><name><surname>Comeau</surname>
<given-names>M R</given-names>
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<contrib contrib-type="author"><name><surname>Friend</surname>
<given-names>D</given-names>
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<contrib contrib-type="author"><name><surname>Thoma</surname>
<given-names>B</given-names>
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<contrib contrib-type="author"><name><surname>Cosman</surname>
<given-names>D</given-names>
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<contrib contrib-type="author"><name><surname>Park</surname>
<given-names>L</given-names>
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<contrib contrib-type="author"><name><surname>Mosley</surname>
<given-names>B</given-names>
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<aff>Immunex Research and Development Corporation, Seattle, WA 98101.</aff>
<pub-date pub-type="ppub"><day>1</day>
<month>2</month>
<year>1994</year>
</pub-date>
<volume>91</volume>
<issue>3</issue>
<fpage>1119</fpage>
<lpage>1123</lpage>
<abstract><p>Specific low-affinity receptors for leukemia inhibitory factor (LIF), oncostatin M (OSM; gp130), and ciliary neurotrophic factor (CNTF; receptor alpha, CNTFR alpha) may be utilized in various combinations to generate high-affinity binding sites and signal transduction. We have tested the ability of combinations of these receptors to transduce a proliferative signal in BAF-B03 cells. Coexpression of the LIF receptor and gp130 in these cells conferred high-affinity LIF and OSM binding and responsiveness to LIF and OSM. These cells also responded to CNTF in the absence of detectable binding. The further addition of CNTFR alpha conferred high-affinity CNTF binding and enhanced responsiveness to CNTF but did not modify responses to LIF or OSM. Coexpression of LIF receptor and CNTFR alpha resulted in a nonfunctional high-affinity binding site. These data are consistent with a role for the CNTFR alpha in enhancing CNTF action but the CNTFR alpha is not absolutely required for CNTF action and suggest a wider range of targets for CNTF.</p>
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