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Respiratory Syncytial Virus NS1 Protein Degrades STAT2 by Inducing SOCS1 Expression
Author(s) -
Xiaodong Xu,
Junwen Zheng,
Kun Zheng,
Hou Yan,
Feng Zhao,
Dongchi Zhao
Publication year - 2014
Publication title -
intervirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.641
H-Index - 61
eISSN - 1423-0100
pISSN - 0300-5526
DOI - 10.1159/000357327
Subject(s) - suppressor of cytokine signaling 1 , stat2 , socs3 , tlr3 , biology , microbiology and biotechnology , interferon , signal transduction , phosphorylation , stat , virology , stat3 , gene , innate immune system , immunology , immune system , biochemistry , suppressor , toll like receptor
Respiratory syncytial virus (RSV) nonstructural protein NS1 (NS1) has been shown to block interferon (IFN)-inducible antiviral signaling. The suppressor of cytokine signaling (SOCS) gene family could utilize a feedback loop to block the activation of the JAK/STAT signaling pathway, further inhibiting the activation of host type I IFN. We evaluated the role of the SOCS1 and SOCS3 genes in this antiviral mechanism.

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