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K Ueki

Researcher at University of Tokyo

Publications -  14
Citations -  5696

K Ueki is an academic researcher from University of Tokyo. The author has contributed to research in topics: Insulin receptor & Insulin receptor substrate. The author has an hindex of 10, co-authored 14 publications receiving 5446 citations.

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Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase

TL;DR: It is shown that phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full- lengths Ad in the liver, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK.
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Insulin signalling and insulin actions in the muscles and livers of insulin-resistant, insulin receptor substrate 1-deficient mice.

TL;DR: IRS-1 plays central roles in two major biological actions of insulin in muscles, glucose transport and protein synthesis, and the degree of compensation for IRS-1 deficiency appears to be correlated with the amount of tyrosine-phosphorylated IRS-2 relative to that of IRS- 1 (in wild-type mice).
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Angiotensin II receptor antagonist TCV-116 induces regression of hypertensive left ventricular hypertrophy in vivo and inhibits the intracellular signaling pathway of stretch-mediated cardiomyocyte hypertrophy in vitro.

TL;DR: The results suggest that the renin-angiotensin system (RAS) is involved in the formation of left ventricular hypertrophy (LVH), and a crucial role of the cardiac RAS in the development of LVH produced by pressure overload.
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The extracellular signal-regulated kinase pathway phosphorylates AML1, an acute myeloid leukemia gene product, and potentially regulates its transactivation ability.

TL;DR: The results showed that AML1 is phosphorylated in vivo on two serine residues within the proline-, serine-, and threonine-rich region, with dependence on the activation of extracellular signal-regulated kinase (ERK) and with interleukin-3 stimulation in a hematopoietic cell line.