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Hiroshi Sakaue

Researcher at University of Tokushima

Publications -  126
Citations -  7303

Hiroshi Sakaue is an academic researcher from University of Tokushima. The author has contributed to research in topics: Adipose tissue & Adipocyte. The author has an hindex of 39, co-authored 114 publications receiving 6649 citations. Previous affiliations of Hiroshi Sakaue include Kindai University & Kobe University.

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Up-regulation of Akt3 in estrogen receptor-deficient breast cancers and androgen-independent prostate cancer lines.

TL;DR: The results indicate that Akt3 may contribute to the more aggressive clinical phenotype of the estrogen receptor-negative breast cancers and androgen-insensitive prostate carcinomas.
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1-Phosphatidylinositol 3-kinase activity is required for insulin-stimulated glucose transport but not for RAS activation in CHO cells.

TL;DR: The stable overexpression in a Chinese hamster ovary (CHO) cell line of a mutant p85 alpha (delta p85) protein, which lacks a binding site for p110, disrupted the complex formation between IRS-1 and the catalytic subunit of PI 3-kinase in intact cells during insulin stimulation, suggesting that PI 3 -kinase is required for glucose transport in insulin signaling in CHO cells.
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Requirement of Atypical Protein Kinase Cλ for Insulin Stimulation of Glucose Uptake but Not for Akt Activation in 3T3-L1 Adipocytes

TL;DR: It is suggested that insulin-elicited signals that pass through PI 3-kinase subsequently diverge into at least two independent pathways, an Akt pathway and a PKCλ pathway, and that the latter pathway contributes, at least in part, to insulin stimulation of glucose uptake in 3T3-L1 adipocytes.
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Involvement of phosphoinositide 3-kinase in insulin- or IGF-1-induced membrane ruffling

TL;DR: The results suggest that the association of IRS‐1 with PI 3‐kinase followed by the activation of PI 3-kinase are required for insulin‐ or IGF‐1‐ induced, but not for EGF‐induced, membrane ruffling.
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Role of STAT-3 in regulation of hepatic gluconeogenic genes and carbohydrate metabolism in vivo

TL;DR: Liver-specific expression of a constitutively active form of STAT-3, achieved by infection with an adenovirus vector, markedly reduced blood glucose, plasma insulin concentrations and hepatic gluconeogenic gene expression in diabetic mice.