Phosphorylation of the Stat1 Transactivation Domain Is Required for Full-Fledged IFN-γ-Dependent Innate Immunity

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Stress-induced phosphorylation of STAT1 at Ser727 requires p38 mitogen-activated protein kinase whereas IFN-γ uses a different signaling pathway

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Ser727‐dependent recruitment of MCM5 by Stat1α in IFN‐γ‐induced transcriptional activation

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Specificity of signaling by STAT1 depends on SH2 and C‐terminal domains that regulate Ser727 phosphorylation, differentially affecting specific target gene expression

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Induction of Apoptosis and Fas Receptor/Fas Ligand Expression by Ischemia/Reperfusion in Cardiac Myocytes Requires Serine 727 of the STAT-1 Transcription Factor but Not Tyrosine 701

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Combinatorial association and abundance of components of interferon-stimulated gene factor 3 dictate the selectivity of interferon responses.

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p38 MAPK enhances STAT1-dependent transcription independently of Ser-727 phosphorylation

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Requirement of Ca 2+ and CaMKII for Stat1 Ser-727 phosphorylation in response to IFN-γ

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Activation of the Transcription Factor ISGF3 by Interferon-gamma

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Stat1-Dependent, p53-Independent Expression of p21 waf1 Modulates Oxysterol-Induced Apoptosis

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Stat1 combines signals derived from IFN‐γ and LPS receptors during macrophage activation

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Stress-induced phosphorylation of STAT1 at Ser727 requires p38 mitogen-activated protein kinase whereas IFN-γ uses a different signaling pathway

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Threonine phosphorylation of STAT1 restricts interferon signaling and promotes innate inflammatory responses

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