NDLI: The Cdk5/p35 kinases modulate leptin-induced STAT3 signaling

Content Provider	PubMed Central
Author	He, Yi Kastin, Abba J. Hung, Hsuchou Pan, Weihong
Abstract	Cyclin dependent kinase (Cdk)-5 is ubiquitously expressed in the brain and plays an essential role in CNS development and synaptic plasticity. The p35 kinase is a neuronal specific activator of Cdk5. Here, we show for the first time that Cdk5 activation modulates leptin signaling. P35 and its metabolite p25 were co-localized with the leptin receptor ObR in selective neurons in the hypothalamus. Overexpression of p35 alone was sufficient to induce the transcriptional activation of Signal Transducer and Activator of Transcription 3 (STAT3) in a cellular model. In retinoic acid-differentiated SH-SY5Y neuronal cells where ObRb was induced, leptin increased the expression of Cdk5, p35, and p25 kinases. The time course of induction coincided with that of phosphorylated (p)-STAT3. When Cdk5 activity was inhibited, either by roscovitine or overexpression of dominant negative Cdk5, there was a reduction of pSTAT3 activation. The results show that the activation of Cdk5 by p35 sustained leptin-induced pSTAT3 at 3 – 6 h. Thus, p35 is a novel modulator of leptin-induced STAT3 signaling.
Related Links	http://dx.doi.org/10.1007/s12031-008-9174-3
Ending Page	58
Page Count	10
Starting Page	49
File Format	PDF
ISSN	08958696
e-ISSN	15591166
Journal	Journal of molecular neuroscience : MN
Issue Number	1-2
Volume Number	39
Language	English
Publisher Date	2009-09-01
Access Restriction	Open
Subject Keyword	Cellular and Molecular Neuroscience Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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