Regulation of insulin signaling via myosin motor protein and actin cytoskeletal network

Creators Nakamori Yoshitaka

Creators Emoto Masahiro

Creators Tanizawa Yukio

Impairment of systemic insulin action causes insufficient glucose uptake to cells and compensatory hyper-secretion of insulin from pancreatic β-cells. This insulin-resistant state promotes development of type 2 diabetes, obesity, hypertension, dyslipidemia, and atherosclerosis. Numerous attempts have been made to clarigy this pathogenesis and molocular mechanisms of insulin resistance. Tumor necrosis factor-α(TNF-α) is one of adipocytokines and a major factor causing insulin resistance. This cytokine attenuates insulin signaling by phosphorylation of insulin receptor substrate-1(IRS-1) Ser residues. However little is known about the precise molecular mechanisms. Recently we reported that IκB kinase-β(IKK-β) interacted with IRS-1, and phosphorylated IRS-1 Ser^<307> through molecular motor and actincytoskeleton. In this review, we overview this unique molecular mechanism and propose a new model that molecular motor and cytoskeletal network organize signaling cross-talk.

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