ADIPOSE TISSUE-SPECIFIC PTEN KNOCKOUT MICE
UCLA Technology Available For Licensing

BACKGROUND:  Aberrant glucose uptake due to insulin resistance is a key pathogenic feature of type 2 diabetes. Insulin signals through its cell surface receptor (IR). The binding of insulin to IR leads to the activation of the PI3-kinase pathway. A phosphatase and tensin homolog deleted from chromosome 10 (PTEN) is a negative regulator of the PI3-kinase/AKT pathway and is hypothesized to inhibit the metabolic effects of insulin. Understanding insulin signaling will lead to new targets for interventions aimed at reversing insulin resistance.

INNOVATION:  UCLA researchers have developed a mouse model to explore the mechanisms by which insulin signaling in adipose tissue regulates systemic insulin sensitivity. A targeted deletion of Pten in adipose tissue was accomplished by utilizing the Cre-lox system under control of the aP2 adipose specific promoter. Loss of Pten results in improved systemic glucose tolerance and insulin sensitivity. In addition, mutant animals exhibit increased insulin signaling and AMP kinase activity in the liver.

POTENTIAL APPLICATIONS:

Related Paper (Selected) Reference: UCLA Case No. 2004-644

For additional technical details and current licensing
availability, please contact the following UCLA office:

UCLA Office of Intellectual Property
11000 Kinross Avenue, Suite #200
Los Angeles, CA 90095-7231
Tel: 310-794-0558 Fax: 310-794-0638
email: ncd@research.ucla.edu
NCD URL:   http://www.research.ucla.edu/tech/ucla05-059.htm

Lead Inventor: Hong Wu

UCLA Technologies Available for Licensing
http://www.research.ucla.edu/oipa/industry

Copyright © 2007 The Regents of the University of California.

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