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Kaoru Yamagata

Researcher at University of Occupational and Environmental Health Japan

Publications -  26
Citations -  964

Kaoru Yamagata is an academic researcher from University of Occupational and Environmental Health Japan. The author has contributed to research in topics: Mesenchymal stem cell & Chromatin immunoprecipitation. The author has an hindex of 13, co-authored 26 publications receiving 681 citations. Previous affiliations of Kaoru Yamagata include Kobe University.

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Cell/tissue-tropic functions of Wnt5a signaling in normal and cancer cells

TL;DR: A model where the outcomes of normal and aberrant Wnt5a/Ror2 signaling depend on cell/tissue-tropic contexts is proposed, with an emphasis on the role of Ror2 in cancer.
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The JAK inhibitor, tofacitinib, reduces the T cell stimulatory capacity of human monocyte-derived dendritic cells

TL;DR: Tofacitinib, a JAK1/JAK3 inhibitor, affected the activities of human DCs and decreased CD80/CD86 expression and T cell stimulatory capability through suppression of type I IFN signalling, suggesting a novel mode of action and a pivotal role for JAKs in the differentiation of DCs.
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Janus Kinase Inhibitor Baricitinib Modulates Human Innate and Adaptive Immune System.

TL;DR: Baricitinib suppresses the differentiation of plasmablasts, Th1 and Th17 cells, as well as innate immunity, such as the T cell stimulatory capacity of dendritic cells, which indicates that JAK inhibitors can be potentially clinically effective not only in rheumatoid arthritis but other immune-related diseases.
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Dissection of Wnt5a-Ror2 Signaling Leading to Matrix Metalloproteinase (MMP-13) Expression

TL;DR: It is shown by reporter assay that the activator protein 1 (AP1) (binding site in the promoter region of MMP-13 gene is primarily responsible for its transcriptional activation by Wnt5a-Ror2 signaling in osteosarcoma cell lines SaOS-2 and U2OS.
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IL-6 and sIL-6R induces STAT3-dependent differentiation of human VSMCs into osteoblast-like cells through JMJD2B-mediated histone demethylation of RUNX2.

TL;DR: The results indicate that the IL-6/STAT3/JMJD2B pathway regulates hVSMCs differentiation into osteoblast-like cells, which suggest its pathogenic role in vascular calcification associated with chronic inflammation.