Biological activities of receptor-interacting protein 140 in adipocytes and metabolic diseases.

Détails

ID Serval
serval:BIB_7926EFF7E0DD
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Biological activities of receptor-interacting protein 140 in adipocytes and metabolic diseases.
Périodique
Current diabetes reviews
Auteur(s)
Ho P.C., Wei L.N.
ISSN
1875-6417 (Electronic)
ISSN-L
1573-3998
Statut éditorial
Publié
Date de publication
11/2012
Peer-reviewed
Oui
Volume
8
Numéro
6
Pages
452-457
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
Receptor-interacting protein 140 (RIP140) is best known for its functional role as a wide-spectrum transcriptional co-regulator. It is highly expressed in metabolic tissues including mature adipocyte. In the past decade, molecular biological and biochemical studies revealed extensive and sequential post-translational modifications (PTMs) of RIP140. Some of these PTMs affect RIP140's sub-cellular distribution and biological activities that contribute to the development and progression of metabolic diseases. The biological activity of RIP140 that translocates to the cytoplasm in adipocytes is to regulate glucose uptake, adiponectin secretion and lipolysis. Accumulation of RIP140 in the cytoplasm promotes adipocyte dysfunctions, and provides a biomarker of early stages of metabolic diseases. Administering compounds that reduce cytoplasmic accumulation of RIP140 in high fat diet-fed animals can ameliorate metabolic dysfunctions, manifested in improving insulin sensitivity and adiponectin secretion, and reducing incidences of hepatic steatosis. This review summarizes studies demonstrating RIP140's PTMs and biological activities in the cytoplasm of adipocyte, signaling pathways stimulating these PTMs, and a proof-of-concept that targeting cytoplasmic RIP140 can be an effective strategy in managing metabolic diseases.
Mots-clé
3T3-L1 Cells/metabolism, Adipocytes/metabolism, Animals, Biomarkers/metabolism, Cytoplasm/metabolism, Diet, High-Fat, Humans, Insulin Resistance, Metabolic Syndrome/genetics, Metabolic Syndrome/metabolism, Methylation, Mice, Mice, Knockout, Nuclear Receptor Co-Repressor 1/genetics, Nuclear Receptor Co-Repressor 1/metabolism, Phosphorylation, Protein Processing, Post-Translational, Signal Transduction
Pubmed
Création de la notice
05/04/2019 16:52
Dernière modification de la notice
20/08/2019 15:35
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