共查询到20条相似文献,搜索用时 31 毫秒
1.
2.
3.
4.
5.
M F Brizzi P Dentelli A Rosso Y Yarden L Pegoraro 《The Journal of biological chemistry》1999,274(24):16965-16972
6.
7.
Association of STATs with relatives and friends 总被引:21,自引:0,他引:21
8.
9.
10.
Nucleocytoplasmic shuttling of STAT transcription factors. 总被引:6,自引:0,他引:6
11.
12.
13.
14.
15.
Fagerlie SR Koretsky T Torok-Storb B Bagby GC 《Journal of immunology (Baltimore, Md. : 1950)》2004,173(6):3863-3870
The Fanconi anemia (FA) group C protein, FANCC, interacts with STAT1 following stimulation with IFN-gamma and is required for proper docking of STAT1 at the IFN-gamma receptor alpha-chain (IFN-gammaRalpha, IFN-gammaR1). Consequently, loss of a functional FANCC results in decreased activation of STAT1 following IFN-gamma stimulation. Because type I IFN receptors influence the function of type II receptors, and vice versa, we conducted experiments designed to determine whether type I IFN-induced activation of other STAT proteins is compromised in FA-C cells and found that activation of STAT 1, 3, and 5 is diminished in type I IFN-stimulated cells bearing Fancc-inactivating mutations. We also determined that the reduced activation of STATs was accompanied by significant reduction of type I IFN-induced tyrosine kinase 2 and Jak1 phosphorylation. Because tyrosine kinase 2 plays a role in differentiation of Th cells, we quantified cytokine secretion from CD4+ cells and in vitro generated CD4+ Th cell subsets from splenocytes of Fancc null mice to that of heterozygous mice and discovered reduced CD4+ IFN-gamma secretion in the Fancc-/- mouse, indicating impaired Th1 differentiation. We suggest that Fancc mutations result in a subtle immunological defect owing to the failure of FANCC to normally support Jak/STAT signaling. 相似文献
16.
17.
Rac1 and a GTPase-activating protein, MgcRacGAP, are required for nuclear translocation of STAT transcription factors 下载免费PDF全文
Kawashima T Bao YC Nomura Y Moon Y Tonozuka Y Minoshima Y Hatori T Tsuchiya A Kiyono M Nosaka T Nakajima H Williams DA Kitamura T 《The Journal of cell biology》2006,175(6):937-946
18.
19.