Journal article
T cell protein tyrosine phosphatase (TCPTP) deficiency in muscle does not alter insulin signalling and glucose homeostasis in mice
K Loh, TL Merry, S Galic, BJ Wu, MJ Watt, S Zhang, ZY Zhang, BG Neel, T Tiganis
Diabetologia | SPRINGER | Published : 2012
Abstract
Aims/hypothesis: Insulin activates insulin receptor protein tyrosine kinase and downstream phosphatidylinositol-3-kinase (PI3K)/Akt signalling in muscle to promote glucose uptake. The insulin receptor can serve as a substrate for the protein tyrosine phosphatase (PTP) 1B and T cell protein tyrosine phosphatase (TCPTP), which share a striking 74% sequence identity in their catalytic domains. PTP1B is a validated therapeutic target for the alleviation of insulin resistance in type 2 diabetes. PTP1B dephosphorylates the insulin receptor in liver and muscle to regulate glucose homeostasis, whereas TCPTP regulates insulin receptor signalling and gluconeogenesis in the liver. In this study we asse..
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Awarded by National Institutes of Health
Funding Acknowledgements
We thank C. Yang and T. Tiganis for technical support. This work was supported by the National Health and Medical Research Council (NHMRC) of Australia (to T. Tiganis and M.J. Watt) and the National Institutes of Health (to Z.-Y. Zhang, RO1 CA126937; and B.G. Neel, R37 CA49152), and by funds from the Ontario Ministry of Health and Long Term Care and the Princess Margaret Hospital Foundation (to B. G. Neel). T. Tiganis and M.J. Watt are NHMRC Research Fellows; B.G. Neel is a Canada Research Chair (Tier I).