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

Mathias Müller, James Briscoe, Carl Laxton, Dmitry Guschin, Andrew Ziemiecki, Olli Silvennoinen, Ailsa G. Harpur, Giovanna Barbieri, Bruce A. Witthuhn, Chris Schindler, Sandra Pellegrini, Andrew F. Wilks, James N. Ihle, George R. Stark, Lan M. Kerr

Research output: Contribution to journalArticlepeer-review

614 Scopus citations

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/beta; 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.

Original languageEnglish (US)
Pages (from-to)129-135
Number of pages7
JournalNature
Volume366
Issue number6451
DOIs
StatePublished - 1993

Bibliographical note

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Copyright 2018 Elsevier B.V., All rights reserved.

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