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Kunikazu Tanji

Researcher at Hirosaki University

Publications -  152
Citations -  10392

Kunikazu Tanji is an academic researcher from Hirosaki University. The author has contributed to research in topics: Dementia with Lewy bodies & Lewy body. The author has an hindex of 38, co-authored 144 publications receiving 9129 citations.

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Alteration of biochemical and pathological properties of TDP-43 protein by a lipid mediator, 15-deoxy-Δ12,14-prostaglandin J2

TL;DR: Biochemical and immunocytochemical analyses showed that 15d-PGJ(2) affects the proteolysis, solubility, and subcellular localization of TDP-43, similar to alterations found in T DP-43 proteinopathy, and suggest that 14-Deoxy-Delta(12,14)-prostaglandin J(2), non-enzymatically produced from PGD(2).
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Alteration of mitochondrial protein PDHA1 in Lewy body disease and PARK14.

TL;DR: PDHA1 is reported as a new component of brainstem-type Lewy bodies in idiopathic PD, DLB and PARK14, the level of PDHA1 protein being significantly decreased in the putamen and substantia nigra of patients with idiopathy PD, suggesting that alteration of glucose metabolism through dysfunction of the PDH complex might occur in the pathogenesis of Lewy body disease and PARK 14.
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Platelet-activating factor enhances the expression of nerve growth factor in normal human astrocytes under hypoxia.

TL;DR: It is concluded that PAF enhances NGF gene expression in human astrocytes, and the PAF-induced increase in the expression of NGF under hypoxia may benefit the protection of the nervous tissue by promoting neuronal survival.
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Gnetin C, a resveratrol dimer, reduces amyloid-β 1-42 (Aβ42) production and ameliorates Aβ42-lowered cell viability in cultured SH-SY5Y human neuroblastoma cells.

TL;DR: Gnetin C may prevent Aβ toxicity by suppressing BACE1 and enhancing MMP-14, together with reducing both internalization and oligomerization of exogenous Aβ monomers, and lead to the prevention of Aβ-mediated diseases, particularly AD.
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Interferon (IFN)-induced protein 35 (IFI35) negatively regulates IFN-β-phosphorylated STAT1-RIG-I-CXCL10/CCL5 axis in U373MG astrocytoma cells treated with polyinosinic-polycytidylic acid.

TL;DR: The results suggest that IFI 35 may negatively regulate the TLR3-IFN-β-P-STAT1-RIG-I-CXCL10/CCL5 axis in U373MG cells, and IFI35 may play a role at least partially in the regulation of innate immune reactions in astrocytes.