Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 112, Issue 2, Pages 488-497Publisher
WILEY
DOI: 10.1002/jcb.22936
Keywords
JAK2; STAT3; C/EBP beta; ADIPOGENESIS
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Funding
- 973 Program [2006CB503900, 2006CB910703]
- National Natural Science Foundation of China [30821065]
- Chinese Academy of Sciences [KSCX1-YW-02, KJCX2-YW-M15]
- Science and Technology Commission of Shanghai Municipality [07dz05907]
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Signal transducer and activator of transcription 3 (STAT3) was reported to be involved in adipogenesis. However, the regulating mechanism of STAT3 remains unclear. The present results showed that STAT3 was activated within 2-h adipogenic induction, in which the phosphorylated STAT3 translocated from cytoplasm to the nucleus. In addition, we detected Janus kinase2 (JAK2) acted upstream of the STAT3 activation at the early stage of adipogenesis. Accordingly, the JAK2 inhibitor AG490 and siRNAs led to the partial inhibition of the STAT3 activation, and the inhibition of 3T3-L1 adipocyte differentiation. Furthermore, the results based on lueiferase, chromatin immunoprecipitation, and gel shift approaches indicated that STAT3 could regulate the transcription of C/EBP beta by binding the distal region of C/EBP beta promoter at the early stage of adipogenesis. Collectively, our findings reveal that JAK2/STAT3 pathway is involved in the early stage of 3T3-L1 adipocyte differentiation though regulating the C/EBP beta transcription. J. Cell. Biochem. 112: 488-497, 2011. (C) 2010 Wiley-Liss, Inc.
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