THE PROTEIN-TYROSINE KINASE JAK1 COMPLEMENTS DEFECTS IN INTERFERON-ALPHA/BETA AND INTERFERON-GAMMA SIGNAL-TRANSDUCTION

被引:730
作者
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
机构
[1] IMPERIAL CANC RES FUND, POB 124, 44 LINCOLNS FIELDS, LONDON WC2A 3PX, ENGLAND
[2] UNIV BERN, INST CLIN & EXPTL CANC RES, CH-3004 BERN, SWITZERLAND
[3] NYU MED CTR, NEW YORK, NY 10016 USA
[4] LUDWIG INST CANC RES, MELBOURNE TUMOUR BIOL BRANCH, MELBOURNE, VIC 3050, AUSTRALIA
[5] INST PASTEUR, INSERM, U276, F-75724 PARIS 15, FRANCE
[6] ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA
[7] COLUMBIA UNIV, MED CTR, DEPT MED, NEW YORK, NY 10032 USA
[8] CLEVELAND CLIN FDN, RES INST, CLEVELAND, OH 44195 USA
关键词
D O I
10.1038/366129a0
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
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页码:129 / 135
页数:7
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