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


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1993-11

AUTHORS

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

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. More... »

PAGES

129-135

Journal

TITLE

Nature

ISSUE

6451

VOLUME

366

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/366129a0

DOI

http://dx.doi.org/10.1038/366129a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053037655

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8232552


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