Sam68 and ERKs regulate leptin-induced expression of OB-Rb mRNA in C2C12 myotubes

P. Maroni, L. Citterio, R. Piccoletti, P. Bendinelli

Research output: Contribution to journalArticlepeer-review


Acute leptin treatment significantly increases the mRNA of the long isoform of leptin receptor (OB-Rb) in C2C12 myotubes after as little as 30 min, 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.

Original languageEnglish
Pages (from-to)26-31
Number of pages6
JournalMolecular and Cellular Endocrinology
Issue number1-2
Publication statusPublished - Oct 15 2009


  • ERKs
  • Leptin
  • Leptin receptor
  • Sam68

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Molecular Biology


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