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Mitsuharu Sato

Researcher at University of Tokyo

Publications -  23
Citations -  6532

Mitsuharu Sato is an academic researcher from University of Tokyo. The author has contributed to research in topics: Transcription factor & Regulation of gene expression. The author has an hindex of 23, co-authored 23 publications receiving 6207 citations. Previous affiliations of Mitsuharu Sato include Osaka University.

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IRF-7 is the master regulator of type-I interferon-dependent immune responses

TL;DR: It is shown that mice deficient in the Irf7 gene are more vulnerable than Myd88-/- mice to viral infection, and this correlates with a marked decrease in serum IFN levels, indicating the importance of the IRF-7-dependent induction of systemic IFN responses for innate antiviral immunity.
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Distinct and Essential Roles of Transcription Factors IRF-3 and IRF-7 in Response to Viruses for IFN-α/β Gene Induction

TL;DR: The results demonstrate the essential and distinct roles of the two factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.
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Positive feedback regulation of type I IFN genes by the IFN-inducible transcription factor IRF-7

TL;DR: Results indicate that IRF‐7 is a key factor in the positive feedback regulation of IFN‐β/β production, and in cells lacking p48, an essential component ofIFN stimulated gene factor 3 (ISGF3).
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Multistage regulation of Th1-type immune responses by the transcription factor IRF-1.

TL;DR: It is shown that T cells from mice lacking the transcription factor IRF-1 fail to mount Th1 responses and instead exclusively undergo Th2 differentiation in vitro, indicating the involvement of IRf-1 in multiple stages of the Th1 limb of the immune response.
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Cross Talk Between Interferon-γ and -α/β Signaling Components in Caveolar Membrane Domains

TL;DR: Induction of cellular responses to cytokines often involves cross-communication through their respective receptors, and here, signaling by interferon-gamma (IFN-Gamma) is shown to depend on the IFN-alpha/beta receptor components.