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Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179]
Previous studies implicate the nonreceptor protein tyrosine kinase (PTK) p59fyn in the propagation of signals from the B cell antigen receptor. To elucidate the functions of this kinase, we examined B cell responsiveness in mice engineered to lack the hematopoietic isoform of p59fyn. Remarkably, ant...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1995
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192161/ https://www.ncbi.nlm.nih.gov/pubmed/7650487 |
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collection | PubMed |
description | Previous studies implicate the nonreceptor protein tyrosine kinase (PTK) p59fyn in the propagation of signals from the B cell antigen receptor. To elucidate the functions of this kinase, we examined B cell responsiveness in mice engineered to lack the hematopoietic isoform of p59fyn. Remarkably, antigen receptor signaling was only modestly defective in fynTnull B cells. In contrast, signaling from the interleukin (IL)-5 receptor which ordinarily provides a comitogenic stimulus with antiimmunoglobulin, was completely blocked. Our results document the importance of p59fynT in IL-5 responses in B cells, and they support a general model for cytokine receptor signal transduction involving the simultaneous recruitment of at least three families of PTK. |
format | Text |
id | pubmed-2192161 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1995 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21921612008-04-16 Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] J Exp Med Articles Previous studies implicate the nonreceptor protein tyrosine kinase (PTK) p59fyn in the propagation of signals from the B cell antigen receptor. To elucidate the functions of this kinase, we examined B cell responsiveness in mice engineered to lack the hematopoietic isoform of p59fyn. Remarkably, antigen receptor signaling was only modestly defective in fynTnull B cells. In contrast, signaling from the interleukin (IL)-5 receptor which ordinarily provides a comitogenic stimulus with antiimmunoglobulin, was completely blocked. Our results document the importance of p59fynT in IL-5 responses in B cells, and they support a general model for cytokine receptor signal transduction involving the simultaneous recruitment of at least three families of PTK. The Rockefeller University Press 1995-09-01 /pmc/articles/PMC2192161/ /pubmed/7650487 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 Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title | Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title_full | Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title_fullStr | Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title_full_unstemmed | Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title_short | Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179] |
title_sort | involvement of p59fynt in interleukin-5 receptor signaling [published erratum appears in j exp med 1995 oct 1;182(4):1179] |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192161/ https://www.ncbi.nlm.nih.gov/pubmed/7650487 |