Parafibromin Is a Component of IFN-γ–Triggered Signaling Pathways That Facilitates JAK1/2-Mediated Tyrosine Phosphorylation of STAT1 | Zendy

Jin Wei | Zendy; Huan Lian | Zendy; Bo Zhong | Zendy; HongBing Shu | Zendy

Open Access

Parafibromin Is a Component of IFN-γ–Triggered Signaling Pathways That Facilitates JAK1/2-Mediated Tyrosine Phosphorylation of STAT1

Author(s) -

Jin Wei,

Huan Lian,

Bo Zhong,

HongBing Shu

Publication year - 2015

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1501111

Subject(s) - stat1 , phosphorylation , tyrosine phosphorylation , microbiology and biotechnology , janus kinase 1 , signal transduction , chemistry , gene knockdown , jak stat signaling pathway , tyrosine , stat , transcription factor , cancer research , biology , janus kinase , biochemistry , gene , stat3 , receptor tyrosine kinase

IFN-γ (also known as type II IFN) is a cytokine that is critically involved in antiviral and immunomodulatory effects. IFN-γ activates JAK1 and JAK2, which lead to the phosphorylation and activation of the transcription factor STAT1. Whether and how additional molecules are involved in the process are not fully clear. In this study, we identified parafibromin as an important component of the IFN-γ-triggered signaling pathways. Overexpression of parafibromin promoted IFN-γ-triggered phosphorylation of STAT1 at Tyr(701), subsequent expression of downstream genes, and cellular antiviral response, whereas knockdown of parafibromin had opposite effects. Parafibromin interacted with JAK1/2, promoted the interactions of JAK1-JAK2 and JAK1/2-STAT1, and promoted tyrosine phosphorylation of STAT1 by JAKs after IFN-γ stimulation. Our results reveal a previously uncharacterized role of parafibromin in mediating IFN-γ-triggered signaling and cellular effects.

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