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Flightless-1, a novel transcriptional modulator of PPARγ through competing with RXRα.

Abstract：

:Peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor family and plays key roles in glucose and lipid metabolism. Its transcriptional control of target genes is mediated by ligand-dependent recruitment of coactivators. In this study, we demonstrate that a novel transcriptional modulator of PPARγ, Flightless-I (FLII) binds directly to and suppresses the transcriptional activity of PPARγ. The LXXLL motif within the leucine-rich repeat (LRR) domain of FLII interacts directly with the DNA-binding domain of PPARγ. Interestingly, in the presence of PPARγ ligands, such as rosiglitazone and SR1664, this interaction was abolished in vitro. When FLII was overexpressed, both the transcriptional activity of PPARγ and adipogenesis were suppressed significantly, whereas specific knockdown of FLII reversed these effects. Furthermore, DNA occupancy of PPARγ on its target gene promoters was enhanced by FLII knockdown, and the interaction between PPARγ and retinoid X receptor α (RXRα) was blocked by FLII. Together, these findings strongly suggest that FLII functions in PPARγ activation as a molecular switch to repress transcriptional activity by interrupting formation of the PPARγ/RXRα complex, and FLII may serve as a novel therapeutic target in the treatment of adiposity-related metabolic syndromes.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Choi JS,Choi SS,Kim ES,Seo YK,Seo JK,Kim EK,Suh PG,Choi JH

doi

10.1016/j.cellsig.2014.11.035

subject

Has Abstract

pub_date

2015-03-01 00:00:00

pages

614-20

issue

3

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(14)00389-1

journal_volume

27

pub_type

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