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Identification of the mechanisms of phosphorylation of PPARy and its relations with the recruitment of corepressors

Grant number: 16/13480-9
Support type:Scholarships in Brazil - Master
Effective date (Start): September 01, 2016
Effective date (End): December 31, 2018
Field of knowledge:Biological Sciences - Biochemistry - Chemistry of Macromolecules
Principal Investigator:Ana Carolina Migliorini Figueira
Grantee:Thaís Helena Tittanegro
Home Institution: Centro Nacional de Pesquisa em Energia e Materiais (CNPEM). Ministério da Ciência, Tecnologia, Inovações e Comunicações (Brasil). Campinas , SP, Brazil
Associated scholarship(s):17/12314-0 - Inhibition of LXR alpha phosphorylation - Evaluating target gene expression effects and LXR alpha and PPAR gamma crosstalk, BE.EP.MS

Abstract

The active peroxisome proliferator-activator receptor ³ (PPAR³) is a potentialtarget for the class of thiazolidinediones (TZD) also known as glitazone, drugs responsible forthis sensitization to insulin in patients with diabetes mellitus type 2. However, its use hasbeen administered with great caution due to its major side effects including weight gain,fluid retention, bone loss, hemodilution, and heart failure appears in more than 15% ofpatients. Recently, studies have demonstrated that the action of the drug occurs mainly byinhibiting cyclin-dependent kinase (Cdk5) conducting the phosphorylation of Ser273 residuePPAR³, improve insulin sensitivity. However, this drug also causes activation of NR resultingin undesirable side effects such as increased adipose tissue by adipogenesis specificallyregulated by PPAR³. In the search for the ideal ligand to NR, opens a wide field of research,where it seeks a molecule able to bind to the PPAR³ without causing its activation, but alsobe able to protect the site of the Ser273 residue against phosphorylation by Cdk5.Therefore, it is necessary to elucidate which the actual correlation between thephosphorylation of the Ser273 residue mechanisms and corepressor recruitmentmechanisms, these recruited as the PPAR³ is not linked to any ligand.

Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)

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