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Yoshiaki Kido

Researcher at RMIT University

Publications -  88
Citations -  5972

Yoshiaki Kido is an academic researcher from RMIT University. The author has contributed to research in topics: Insulin receptor & Insulin. The author has an hindex of 36, co-authored 84 publications receiving 5485 citations. Previous affiliations of Yoshiaki Kido include Kobe University & National Institutes of Health.

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The forkhead transcription factor Foxo1 links insulin signaling to Pdx1 regulation of pancreatic β cell growth

TL;DR: It is proposed that insulin/IGFs regulate beta cell proliferation by relieving Foxo1 inhibition of Pdx1 expression in a subset of cells embedded within pancreatic ducts.
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Distinct and Overlapping Functions of Insulin and IGF-I Receptors

TL;DR: Evidence from genetically engineered mice does not support the view that insulin and IGF receptors promote cellular differentiation in vivo or that they are required for early embryonic development, and the phenotypes of insulin receptor gene mutations in humans and in mice indicate important differences between the developmental roles of insulin and its receptor in the two species.
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Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2

TL;DR: Tissue-specific differences in the roles of IRSs to mediate insulin action are indicated, with irs-1 playing a prominent role in skeletal muscle and irS-2 in liver and ir/irs-2(+/-) mice developing severe insulin resistance in liver, with compensatory beta-cell hyperplasia.
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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.
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Clinical review 125: The insulin receptor and its cellular targets.

TL;DR: The presence of multiple insulin-regulated, PIP3-dependent kinases is consistent with the possibility that different pathways are required to regulate different biological actions of insulin.