title: Pin1 enhances adipocyte differentiation by positively regulating the transcriptional activity of PPARγ.
abstract: Pin1 is a peptidylprolyl cis/trans isomerase and it has a unique enzymatic activity of catalyzing isomerization of the peptide bond between phospho-serine/threonine and proline. Through the conformational change of its substrates, Pin1 regulates diverse biological processes including adipogenesis. In mouse embryonic fibroblasts and 3T3-L1 preadipocytes, overexpression of Pin1 enhances adipocyte differentiation whereas inhibition of Pin1 activity suppresses it. However, the precise functions of Pin1 during adipogenesis are not clear. In the present study, we investigated the potential targets of Pin1 during adipogenesis. We found that Pin1 interacts directly with and regulates the transcriptional activity of PPARγ, a key regulator of adipogenesis. In addition, ERK activity and Ser273 of PPARγ, a potential ERK phosphorylation target site, are important for the regulation of PPARγ function by Pin1 in 3T3-L1 cells. Taken together our results suggest a novel regulatory mechanism of Pin1 during adipogenesis, in which Pin1 enhances adipocyte differentiation by regulating the function of PPARγ.
authors.affiliation: College of Pharmacy & Research Institute of Drug Development, Chonnam National University, Gwangju 61186, Republic of Korea.
authors.forename: Younho
authors.initials: Y
authors.lastname: Han
authors.affiliation: College of Pharmacy & Research Institute of Drug Development, Chonnam National University, Gwangju 61186, Republic of Korea.
authors.forename: Sung Ho
authors.initials: SH
authors.lastname: Lee
authors.affiliation: Department of Life Science, Ewha Womans University, Seoul 03760, Republic of Korea.
authors.forename: Minjin
authors.initials: M
authors.lastname: Bahn
authors.affiliation: Department of Life Science, Ewha Womans University, Seoul 03760, Republic of Korea. Electronic address: cyeo@ewha.ac.kr.
authors.forename: Chang-Yeol
authors.initials: CY
authors.lastname: Yeo
authors.affiliation: College of Pharmacy & Research Institute of Drug Development, Chonnam National University, Gwangju 61186, Republic of Korea. Electronic address: kwanglee@chonnam.ac.kr.
authors.forename: Kwang Youl
authors.initials: KY
authors.lastname: Lee
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002070:Butadienes / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects; D051379:Mice; D000072340:NIMA-Interacting Peptidylprolyl Isomerase / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D047495:PPAR gamma / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D011485:Protein Binding / Q000187:drug effects / Q000235:genetics; D012694:Serine / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D002070:Butadienes; D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D009570:Nitriles; D047495:PPAR gamma; C113580:U 0126; D012694:Serine; D048049:Extracellular Signal-Regulated MAP Kinases; C000606850:Pin1 protein, mouse
keywords: Adipogenesis; ERK; PPARγ; Pin1