Müller M, Briscoe J, Laxton C, Guschin D, Ziemiecki A, Silvennoinen O, Harpur A G, Barbieri G, Witthuhn B A, Schindler C
Imperial Cancer Research Fund Laboratories, London, UK.
Nature. 1993 Nov 11;366(6451):129-35. doi: 10.1038/366129a0.
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.
我们构建了一种细胞系，该细胞系缺乏蛋白酪氨酸激酶JAK1，且在干扰素应答方面完全存在缺陷。用JAK1对该突变体进行互补可恢复应答，这确立了JAK1在α/β干扰素和γ干扰素信号转导途径中的必要性。在α干扰素途径中JAK1与Tyk2活性之间以及在γ干扰素途径中JAK1与JAK2之间的相互依存关系，可能反映了这些激酶在干扰素受体复合物正确组装中的必要性。
