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Kazutomo Imahori

Researcher at Mitsubishi

Publications -  46
Citations -  4017

Kazutomo Imahori is an academic researcher from Mitsubishi. The author has contributed to research in topics: Tau protein & GSK-3. The author has an hindex of 30, co-authored 46 publications receiving 3918 citations. Previous affiliations of Kazutomo Imahori include University of Tokyo.

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Journal ArticleDOI

Glycogen synthase kinase 3β is identical to tau protein kinase I generating several epitopes of paired helical filaments

TL;DR: The amino acid sequence of TPKI is presented, which is identical to glycogen synthase kinase 3β (GSK3β), and it is found that TPKI activity was inseparable from GSK3 activity throughout the purification procedure.
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Tau protein kinase I converts normal tau protein into A68-like component of paired helical filaments.

TL;DR: TPKI was more effective than TPKII for producing the decrease of tau-1 immunoreactivity and mobility shift of t Tau on SDS-PAGE, and findings suggested that tau phosphorylated by TPKI resembled A-68, a component of paired helical filaments.
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Preferential labeling of Alzheimer neurofibrillary tangles with antisera for tau protein kinase (TPK) I/glycogen synthase kinase-3 beta and cyclin-dependent kinase 5, a component of TPK II

TL;DR: Findings suggest that cyclin-dependent kinase (cdk) 5 and TPK I/GSK-3β are the critically important kinases for the generation in vivo of hyperphosphorylated tau, the main component of the paired helical filaments in NFT.
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A cdc2-related kinase PSSALRE/cdk5 is homologous with the 30 kDa subunit of tau protein kinase II, a proline-directed protein kinase associated with microtubule

TL;DR: The amino acid sequence of the 30 kDa subunit of TPKII was determined and found it to be homologous with a cdc2‐related kinase, PSSALRE/cdk5, and this result supports the previous hypothesis that the kinase works actively in juvenile brain.
Journal Article

Physiology and Pathology of Tau Protein Kinases in Relation to Alzheimer's Disease

TL;DR: Double staining for either TPKI or TPKII and NFT in the brain of Down's syndrome patients clearly demonstrated that TPKI and TPK II are both associated with NFTIn vivo, suggesting that the level of TPKI/TPKII is elevated in AD brain by some mechanism.