Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 8, Pages 5483-5489Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.8.5483
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Funding
- NIAID NIH HHS [AI 058211, 5T32 AI07525] Funding Source: Medline
- NIGMS NIH HHS [5T32 GM 07367] Funding Source: Medline
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Mammalian type I IFNs (IFN-Is) mediate their potent biological activities through an evolutionarily conserved IFN-alpha receptor (IFNAR), consisting of IFNAR1 and IFNAR2. These two chains direct the rapid activation of two founding members of the STAT family of transcription factors, STAT1 and STAT2. To understand how IFN-Is direct the recruitment and activation of STATs, a series of mutant murine IFNAR1 and IFNAR2 receptors were generated and evaluated in IFNAR1 and IFNAR2 knockout cells. These studies reveal that a single conserved IFNAR2 tyrosine, Y-510, plays a critical role in directing the IFN-I-dependent activation of STAT1 and STAT2, both in murine fibroblasts and macrophages. A second IFNAR2 tyrosine, Y-335, plays a more minor role. Likewise, Y-510 > Y-335 play a critical role in the induction of genes and antiviral activity traditionally associated with IFN-Is.
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