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
Hauptverfasser: 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
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container_end_page 135
container_issue 6451
container_start_page 129
container_title Nature (London)
container_volume 366
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. 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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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