Structural basis of a unique interferon-β signaling axis mediated via the receptor IFNAR1

被引:0
|
作者
Nicole A de Weerd
Julian P Vivian
Thao K Nguyen
Niamh E Mangan
Jodee A Gould
Susie-Jane Braniff
Leyla Zaker-Tabrizi
Ka Yee Fung
Samuel C Forster
Travis Beddoe
Hugh H Reid
Jamie Rossjohn
Paul J Hertzog
机构
[1] Centre for Innate Immunity and Infectious Diseases,Department of Biochemistry and Molecular Biology
[2] Monash Institute of Medical Research,undefined
[3] Monash University,undefined
[4] School of Biomedical Sciences,undefined
[5] Monash University,undefined
[6] Australian Research Council Centre of Excellence in Structural and Functional Microbial Genomics,undefined
[7] Monash University,undefined
[8] Institute of Infection and Immunity,undefined
[9] Cardiff University,undefined
[10] School of Medicine,undefined
[11] Heath Park,undefined
[12] Institute of Infection and Immunity,undefined
[13] Cardiff University,undefined
[14] School of Medicine,undefined
[15] Heath Park,undefined
来源
Nature Immunology | 2013年 / 14卷
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学科分类号
摘要
Type I interferons regulate immune responses by signaling via heterodimeric IFNAR1-IFNAR2 complexes. Hertzog and colleagues reveal a unique IFN-β–IFNAR1 signaling complex that is IFNAR2-independent and modulates expression of a distinct set of interferon-inducible genes.
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页码:901 / 907
页数:6
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