The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ signal transduction
We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-alpha/beta and -gamma signal transduction pathway...
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Veröffentlicht in: | Nature (London) 1993-11, Vol.366 (6451), p.129-135 |
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creator | Müller, Mathias Briscoe, James Laxton, Carl Guschin, Dmitry Ziemiecki, Andrew Silvennoinen, Olli Harpur, Ailsa G Barbieri, Giovanna Witthuhn, Bruce A Schindler, Chris Pellegrini, Sandra Wilks, Andrew F Ihle, James N Stark, George R Kerr, lan M |
description | We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes. |
doi_str_mv | 10.1038/366129a0 |
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Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/366129a0</identifier><identifier>PMID: 8232552</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing</publisher><subject>Animals ; Biochemistry ; Biological and medical sciences ; Cell Line ; Cell physiology ; Cellular biology ; DNA-Binding Proteins - metabolism ; Fundamental and applied biological sciences. Psychology ; Genetic Complementation Test ; Humans ; Interferon-alpha - metabolism ; Interferon-beta - metabolism ; Interferon-gamma - metabolism ; Interferon-Stimulated Gene Factor 3 ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; Janus Kinase 1 ; Janus Kinase 2 ; Mice ; Molecular and cellular biology ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; Proteins ; Proteins - metabolism ; Proto-Oncogene Proteins ; Signal Transduction ; STAT1 Transcription Factor ; Trans-Activators ; Transcription Factors - metabolism ; Transcription, Genetic ; TYK2 Kinase ; Tyrosine - metabolism</subject><ispartof>Nature (London), 1993-11, Vol.366 (6451), p.129-135</ispartof><rights>1994 INIST-CNRS</rights><rights>Copyright Macmillan Journals Ltd. 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Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell physiology</subject><subject>Cellular biology</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Fundamental and applied biological sciences. 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Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.</abstract><cop>London</cop><pub>Nature Publishing</pub><pmid>8232552</pmid><doi>10.1038/366129a0</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Biochemistry Biological and medical sciences Cell Line Cell physiology Cellular biology DNA-Binding Proteins - metabolism Fundamental and applied biological sciences. Psychology Genetic Complementation Test Humans Interferon-alpha - metabolism Interferon-beta - metabolism Interferon-gamma - metabolism Interferon-Stimulated Gene Factor 3 Interferon-Stimulated Gene Factor 3, gamma Subunit Janus Kinase 1 Janus Kinase 2 Mice Molecular and cellular biology Mutation Phosphorylation Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Proteins Proteins - metabolism Proto-Oncogene Proteins Signal Transduction STAT1 Transcription Factor Trans-Activators Transcription Factors - metabolism Transcription, Genetic TYK2 Kinase Tyrosine - metabolism |
title | The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ signal transduction |
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