NDLI: WNK1 kinase is essential for insulin‐stimulated GLUT4 trafficking in skeletal muscle

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WNK1 kinase is essential for insulin‐stimulated GLUT4 trafficking in skeletal muscle

Content Provider	Semantic Scholar
Author	Kim, Ji‐ Hee Kim, Hanul Hwang, Kyu‐ Hee Chang, Jae Seung Park, Kyu‐ Sang Cha, Seung‐ Kuy
Copyright Year	2018
Abstract	With-no-lysine 1 (WNK1) kinase is a substrate of the insulin receptor/Akt pathway. Impaired insulin signaling in skeletal muscle disturbs glucose transporter 4 (GLUT4) translocation associated with the onset of type 2 diabetes (T2D). WNK1 is highly expressed in skeletal muscle. However, it is currently unknown how insulin signaling targeting WNK1 regulates GLUT4 trafficking in skeletal muscle, and whether this regulation is perturbed in T2D. Hereby, we show that insulin phosphorylates WNK1 at its activating site via a phosphatidylinositol 3-kinase-dependent mechanism. WNK1 promotes the cell surface abundance of GLUT4 via regulating TBC1D4. Of note, we observed insulin resistance and decreased WNK1 phosphorylation in T2D db/db mice as compared to the control mice. These results provide a new perspective on WNK1 function in the pathogenesis of hyperglycemia in T2D.
Starting Page	1866
Ending Page	1874
Page Count	9
File Format	PDF HTM / HTML
PubMed reference number	30410865v1
Alternate Webpage(s)	https://doi.org/10.1002/2211-5463.12528
DOI	10.1002/2211-5463.12528
Journal	FEBS open bio
Volume Number	8
Language	English
Access Restriction	Open
Subject Keyword	1-Phosphatidylinositol 3-Kinase Diabetes Mellitus Diabetes Mellitus, Non-Insulin-Dependent Glucose Transporter Hyperglycemia Insulin Resistance Lysine Proto-Oncogene Proteins c-akt SLC2A4 gene Skeletal muscle structure WNK1 gene cellular targeting db/db Mouse
Content Type	Text
Resource Type	Article

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