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Michiaki Kohno

Researcher at Gifu Pharmaceutical University

Publications -  24
Citations -  2162

Michiaki Kohno is an academic researcher from Gifu Pharmaceutical University. The author has contributed to research in topics: Mitogen-activated protein kinase & Platelet-derived growth factor receptor. The author has an hindex of 18, co-authored 24 publications receiving 2137 citations. Previous affiliations of Michiaki Kohno include University of Washington & Kyoto University.

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Constitutive activation of the 41-/43-kDa mitogen-activated protein kinase signaling pathway in human tumors

TL;DR: The results suggest that the constitutive activation of 41-/43-kDa MAP kinases in tumor cells is not due to the disorder of MAP kinase themselves, but is due toThe disorder of Raf-1, Ras, or some other signaling molecules upstream of Ras.
Journal Article

Constitutive activation of mitogen-activated protein (MAP) kinases in human renal cell carcinoma.

TL;DR: The results suggest that constitutive activation of MAPKs may be associated with the carcinogenesis of human RCCs.
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Specific activation of the p38 mitogen-activated protein kinase signaling pathway and induction of neurite outgrowth in PC12 cells by bone morphogenetic protein-2.

TL;DR: The results clearly indicate that activation of the p38 MAP kinase pathway is necessary for BMP-2-induced neuronal differentiation of PC12 cells and suggest thatactivation of thep38 MAP Kinase pathway alone can induce the neuronal differentiate of PC 12 cells.
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Tumor necrosis factor stimulates the synthesis and secretion of biologically active nerve growth factor in non-neuronal cells.

TL;DR: It is suggested that TNF plays a role in regulating neuronal cell function through an indirect mechanism by which it stimulates NGF production in glial cells and fibroblasts.
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Activation of the 41/43 kDa mitogen-activated protein kinase signaling pathway is required for hepatocyte growth factor-induced cell scattering

TL;DR: In this paper, the authors showed that activation of the 41/43 kDa MAP kinase signaling pathway is required for motility response of MDCK and TMK1 cells induced by agents such as HGF, PMA and EGF.