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The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ signal transduction

Nature volume 366, pages 129–135 (1993)Cite this article

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-α/β and -γ signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-α pathway, and between JAK1 and JAK2 in the interferon-γ pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.

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Authors and Affiliations

  1. Imperial Cancer Research Fund Laboratories, PO Box 123, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK

    Mathias Müller, James Briscoe, Carl Laxton, Dmitry Guschin & lan M. Kerr

  2. Institute for Clinical and Experimental Cancer Research, University of Berne, Tiefenaustrasse 120, 3004, Berne, Switzerland

    Andrew Ziemiecki

  3. Pharmacology, New York University Medical Center, New York, New York, 10016, USA

    Olli Silvennoinen

  4. Melbourne Tumour Biology Branch, Ludwig Institute for Cancer Research, Victoria, 3050, Australia

    Ailsa G. Harpur & Andrew F. Wilks

  5. Unité INSERM 276, Institut Pasteur, 75724, Paris, Cedex 15, France

    Giovanna Barbieri & Sandra Pellegrini

  6. Biochemistry, St Jude Children's Research Hospital, 322 North Lauderdale, Memphis, Tennesee, 38101-0318, USA

    Bruce A. Witthuhn & James N. Ihle

  7. Department of Medicine, Columbia University Medical Center, New York, New York, 10032, USA

    Chris Schindler

  8. Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio, 44195, USA

    George R. Stark

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  1. Mathias Müller
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Müller, M., Briscoe, J., Laxton, C. et al. The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ signal transduction. Nature 366, 129–135 (1993). https://doi.org/10.1038/366129a0

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