| Literature DB >> 8232552 |
M Müller1, J Briscoe, C Laxton, D Guschin, A Ziemiecki, O Silvennoinen, A G Harpur, G Barbieri, B A Witthuhn, C Schindler.
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.Entities:
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Year: 1993 PMID: 8232552 DOI: 10.1038/366129a0
Source DB: PubMed Journal: Nature ISSN: 0028-0836 Impact factor: 49.962