NDLI: A novel leptin signalling pathway via PTEN inhibition in hypothalamic cell lines and pancreatic β-cells

Content Provider	PubMed Central
Author	Ning, Ke Miller, Lisa C. Laidlaw, Hilary A. Burgess, Laura A. Perera, Nevin M. Downes, C. Peter Leslie, Nick R. Ashford, Michael Lj
Copyright Year	2006
Abstract	In obesity and diabetes, the ability of hypothalamic neurons to sense and transduce changes in leptin and insulin levels is compromised. The effects of both hormones require intracellular signalling via the PI3-kinase pathway, which is inhibited by the phosphatase PTEN. We show that leptin-stimulated F-actin depolymerization in mouse hypothalamic cells is inhibited by PTEN, a process involving independent effects of both its lipid and protein phosphatase activities. Potentially mediating this F-actin depolymerization, leptin, but not insulin, stimulated the phosphorylation of PTEN in a CK2 dependent manner, and inhibited its phosphatase activity. Similarly, hyperpolarization of mouse pancreatic β-cells by leptin also requires coincident PtdIns(3,4,5)P3 generation and actin depolymerization, and could be inhibited by mechanisms requiring both the lipid and protein phosphatase activities of PTEN. These results demonstrate a critical role for PTEN in leptin signalling and indicate a mechanism by which leptin and insulin can produce PI3K dependent differential cellular outputs.
Related Links	http://dx.doi.org/10.1038/sj.emboj.7601118
Ending Page	2387
Page Count	11
Starting Page	2377
File Format	PDF
ISSN	02614189
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	11
Volume Number	25
Language	English
Publisher Date	2006-06-07
Access Restriction	Open
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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