Parafibromin Is a Component of IFN-γ–Triggered Signaling Pathways That Facilitates JAK1/2-Mediated Tyrosine Phosphorylation of STAT1
Copyright policy )Parafibromin Is a Component of IFN-γ–Triggered Signaling Pathways That Facilitates JAK1/2-Mediated Tyrosine Phosphorylation of STAT1
Abstract 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 Tyr701, 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.
- Medical Research Institute Sri Lanka
- Second Military Medical University China (People's Republic of)
- Wuhan University China (People's Republic of)
Tumor Suppressor Proteins, Janus Kinase 1, Janus Kinase 2, Cell Line, DNA-Binding Proteins, Enzyme Activation, Interferon-gamma, HEK293 Cells, STAT1 Transcription Factor, Humans, RNA Interference, Phosphorylation, RNA, Small Interfering, Signal Transduction
Tumor Suppressor Proteins, Janus Kinase 1, Janus Kinase 2, Cell Line, DNA-Binding Proteins, Enzyme Activation, Interferon-gamma, HEK293 Cells, STAT1 Transcription Factor, Humans, RNA Interference, Phosphorylation, RNA, Small Interfering, Signal Transduction
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