| Sam68 and ERKs regulate leptin-induced expression of OB-Rb mRNA in C2C12 myotubes. | |
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MedLine Citation:
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PMID: 19524014 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Acute leptin treatment significantly increases the mRNA of the long isoform of leptin receptor (OB-Rb) in C2C12 myotubes after as little as 30min, without affecting that of the short isoform (OB-Ra). The Sam68 STAR protein has been implicated in leptin signal transduction as an adaptor molecule useful to recruit other signalling proteins. We found that leptin increased Sam68 tyrosine-phosphorylation so decreasing its poly(U)-binding capacity. RT-PCR analysis of the mRNA bound to immunoprecipitated Sam68 showed that Sam68 associated with OB-Rb but not OB-Ra mRNA in control and leptin-treated C2C12 cells. The siRNA-mediated silencing of Sam68 reduced its levels by 89% and abolished the leptin-mediated increase in OB-Rb mRNA. Leptin activates ERKs which in turn might phosphorylate Sam68 modifying its influence on mRNA. We did not observe any changes in Sam68 Ser/Thr phosphorylation but using the specific MEK1 inhibitor PD-98059 showed that leptin-mediated ERK activation is essential for leptin's effect on OB-Rb mRNA expression. Thus it appears that leptin has a positive short-term effect on the regulation of OB-Rb mRNA in C2C12 cells, involving both Sam68 and ERKs. These results might suggest that leptin signal acutely favours its own sensitivity. |
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Authors:
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P Maroni; L Citterio; R Piccoletti; P Bendinelli |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-06-11 |
Journal Detail:
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Title: Molecular and cellular endocrinology Volume: 309 ISSN: 1872-8057 ISO Abbreviation: Mol. Cell. Endocrinol. Publication Date: 2009 Oct |
Date Detail:
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Created Date: 2009-08-03 Completed Date: 2009-10-26 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 7500844 Medline TA: Mol Cell Endocrinol Country: Ireland |
Other Details:
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Languages: eng Pagination: 26-31 Citation Subset: IM |
Affiliation:
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Istituto Ortopedico Galeazzi, IRCCS, Milan, Italy. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Signal Transducing
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metabolism* Animals Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors, metabolism* Gene Expression Regulation / drug effects* Humans Leptin / pharmacology* Mice Muscle Fibers, Skeletal / drug effects*, enzymology* Phosphotyrosine / metabolism Poly U / metabolism Protein Isoforms / genetics, metabolism Protein Kinase Inhibitors / pharmacology RNA, Messenger / genetics, metabolism RNA-Binding Proteins / metabolism* Receptors, Leptin / genetics*, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Signal Transducing; 0/Khdrbs1 protein, mouse; 0/Leptin; 0/Protein Isoforms; 0/Protein Kinase Inhibitors; 0/RNA, Messenger; 0/RNA-Binding Proteins; 0/Receptors, Leptin; 21820-51-9/Phosphotyrosine; 27416-86-0/Poly U; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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