Title |
T cell protein tyrosine phosphatase (TCPTP) deficiency in muscle does not alter insulin signalling and glucose homeostasis in mice
|
---|---|
Published in |
Diabetologia, November 2011
|
DOI | 10.1007/s00125-011-2386-z |
Pubmed ID | |
Authors |
K. Loh, T. L. Merry, S. Galic, B. J. Wu, M. J. Watt, S. Zhang, Z.-Y. Zhang, B. G. Neel, T. Tiganis |
Abstract |
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 assessed for the first time the role of TCPTP in the regulation of insulin receptor signalling in muscle. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 16 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Researcher | 4 | 25% |
Student > Ph. D. Student | 3 | 19% |
Student > Bachelor | 1 | 6% |
Unspecified | 1 | 6% |
Student > Master | 1 | 6% |
Other | 1 | 6% |
Unknown | 5 | 31% |
Readers by discipline | Count | As % |
---|---|---|
Agricultural and Biological Sciences | 4 | 25% |
Biochemistry, Genetics and Molecular Biology | 3 | 19% |
Medicine and Dentistry | 2 | 13% |
Chemistry | 1 | 6% |
Unspecified | 1 | 6% |
Other | 0 | 0% |
Unknown | 5 | 31% |