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IRF4 is a key thermogenic transcriptional partner of PGC-1alpha.

Authors: Kong, X  Banks, A  Liu, T  Kazak, L  Rao, RR  Cohen, P  Wang, X  Yu, S  Lo, JC  Tseng, YH  Cypess, AM  Xue, R  Kleiner, S  Kang, S  Spiegelman, BM  Rosen, ED 
Citation: Kong X, etal., Cell. 2014 Jul 3;158(1):69-83. doi: 10.1016/j.cell.2014.04.049.
Pubmed: (View Article at PubMed) PMID:24995979
DOI: Full-text: DOI:10.1016/j.cell.2014.04.049

Brown fat can reduce obesity through the dissipation of calories as heat. Control of thermogenic gene expression occurs via the induction of various coactivators, most notably PGC-1alpha. In contrast, the transcription factor partner(s) of these cofactors are poorly described. Here, we identify interferon regulatory factor 4 (IRF4) as a dominant transcriptional effector of thermogenesis. IRF4 is induced by cold and cAMP in adipocytes and is sufficient to promote increased thermogenic gene expression, energy expenditure, and cold tolerance. Conversely, knockout of IRF4 in UCP1(+) cells causes reduced thermogenic gene expression and energy expenditure, obesity, and cold intolerance. IRF4 also induces the expression of PGC-1alpha and PRDM16 and interacts with PGC-1alpha, driving Ucp1 expression. Finally, cold, beta-agonists, or forced expression of PGC-1alpha are unable to cause thermogenic gene expression in the absence of IRF4. These studies establish IRF4 as a transcriptional driver of a program of thermogenic gene expression and energy expenditure.


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RGD Object Information
RGD ID: 11564742
Created: 2016-11-16
Species: All species
Last Modified: 2016-11-16
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.