The protein tyrosine kinase JAK1 complements defects in interferon-a/b and -g signal transduction. (Articolo in rivista)

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  • The protein tyrosine kinase JAK1 complements defects in interferon-a/b and -g signal transduction. (Articolo in rivista) (literal)
Anno
  • 1993-01-01T00:00:00+01:00 (literal)
Alternative label
  • Muller M*, Briscoe J *, Laxton C *, Guschin D *, Ziemiecki A +, Silvennoinen O °, Harpur AG §, Barbieri G ^, Witthuhn BA ¶, Schindler C #, Pellegrini S ^, Wilks AF §, Ihle JN ¶, Stark GR ** & Kerr IM * (1993)
    The protein tyrosine kinase JAK1 complements defects in interferon-a/b and -g signal transduction.
    in Nature (Lond.); Macmillan,, London (Regno Unito)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Muller M*, Briscoe J *, Laxton C *, Guschin D *, Ziemiecki A +, Silvennoinen O °, Harpur AG §, Barbieri G ^, Witthuhn BA ¶, Schindler C #, Pellegrini S ^, Wilks AF §, Ihle JN ¶, Stark GR ** & Kerr IM * (literal)
Pagina inizio
  • 129 (literal)
Pagina fine
  • 135 (literal)
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  • 366 (literal)
Rivista
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  • 7 (literal)
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  • 6451 (literal)
Note
  • Google Scholar (literal)
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  • *Imperial Cancer Research Fund Laboratories, PO Box 123, 44 Lincoln's Inn Fields, London WC2A 3PX, UK; +Institute for Clinical and Experimental Cancer Research, University of Berne, Tiefenaustrasse 120, 3004 Berne, Switzerland; °Pharmacology, New York University Medical Center, New York, New York 10016, USA; §Melbourne Tumour Biology Branch, Ludwig Institute for Cancer Research, Victoria 3050, Australia; ^Unité INSERM 276, Institut Pasteur, 75724 Paris, Cedex 15, France; ¶Biochemistry, St Jude Children's Research Hospital, 322 North Lauderdale, Memphis, Tennesee 38101-0318, USA; #Department of Medicine, Columbia University Medical Center, New York, New York 10032, USA; **Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. (literal)
Titolo
  • The protein tyrosine kinase JAK1 complements defects in interferon-a/b and -g signal transduction. (literal)
Abstract
  • 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. (literal)
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