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
Format:	Artikel
Sprache:	eng
Schlagworte:	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
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