Inhibition of C1-Ten PTPase activity reduces insulin resistance through IRS-1 and AMPK pathways-Reference-Cited by-同舟云学术

Inhibition of C1-Ten PTPase activity reduces insulin resistance through IRS-1 and AMPK pathways

Published:2017-12 Issue:1 Volume:7 Page:
ISSN:2045-2322
Container-title:Scientific Reports
language:en
Short-container-title:Sci Rep

Author:

Jeong Heeyoon,Koh Ara,Lee Jiyoun,Park Dohyun,Lee Jung Ok,Lee Mi Nam,Jo Kyung-Jin,Tran Huynh Nguyen Khanh,Kim Eui,Min Byung-Sun,Kim Hyeon Soo,Berggren Per-Olof,Ryu Sung Ho

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/s41598-017-18081-8.pdf

Reference37 articles.

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2. Kerouz, N. J., Horsch, D., Pons, S. & Kahn, C. R. Differential regulation of insulin receptor substrates-1 and -2 (IRS-1 and IRS-2) and phosphatidylinositol 3-kinase isoforms in liver and muscle of the obese diabetic (ob/ob) mouse. The Journal of clinical investigation 100, 3164–3172, https://doi.org/10.1172/JCI119872 (1997).

3. Koh, A. et al. C1-Ten is a protein tyrosine phosphatase of insulin receptor substrate 1 (IRS-1), regulating IRS-1 stability and muscle atrophy. Molecular and cellular biology 33, 1608–1620, https://doi.org/10.1128/MCB.01447-12 (2013).

4. Krook, A. et al. Characterization of signal transduction and glucose transport in skeletal muscle from type 2 diabetic patients. Diabetes 49, 284–292 (2000).

5. Bjornholm, M., Kawano, Y., Lehtihet, M. & Zierath, J. R. Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation. Diabetes 46, 524–527 (1997).

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