The G0/G1 switch gene 2 is a novel PPAR target gene.

Zandbergen, Fokko; Mandard, Stéphane; Escher, Pascal; Tan, Nguan Soon; Patsouris, David; Jatkoe, Tim; Rojas-Caro, Sandra; Madore, Steve; Wahli, Walter; Tafuri, Sherrie; Müller, Michael; Kersten, Sander (2005). The G0/G1 switch gene 2 is a novel PPAR target gene. Biochemical journal, 392(Pt 2), pp. 313-324. Portland Press 10.1042/BJ20050636

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PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha-null mice using microarrays, a novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2), was identified. Hepatic expression of G0S2 was up-regulated by fasting and by the PPARalpha agonist Wy14643 in a PPARalpha-dependent manner. Surprisingly, the G0S2 mRNA level was highest in brown and white adipose tissue and was greatly up-regulated during mouse 3T3-L1 and human SGBS (Simpson-Golabi-Behmel syndrome) adipogenesis. Transactivation, gel shift and chromatin immunoprecipitation assays indicated that G0S2 is a direct PPARgamma and probable PPARalpha target gene with a functional PPRE (PPAR-responsive element) in its promoter. Up-regulation of G0S2 mRNA seemed to be specific for adipogenesis, and was not observed during osteogenesis or myogenesis. In 3T3-L1 fibroblasts, expression of G0S2 was associated with growth arrest, which is required for 3T3-L1 adipogenesis. Together, these data indicate that G0S2 is a novel target gene of PPARs that may be involved in adipocyte differentiation.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Ophthalmology

UniBE Contributor:

Escher, Pascal

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0264-6021

Publisher:

Portland Press

Language:

English

Submitter:

PD Dr. Pascal Escher

Date Deposited:

10 Jul 2017 16:06

Last Modified:

31 Jul 2017 08:31

Publisher DOI:

10.1042/BJ20050636

PubMed ID:

16086669

BORIS DOI:

10.7892/boris.101759

URI:

https://boris.unibe.ch/id/eprint/101759

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