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TP53INP2 regulates adiposity by activating β-catenin through autophagy-dependent sequestration of GSK3β

Journal article
Authors M. Romero
A. Sabaté-Pérez
V. A. Francis
I. Castrillón-Rodriguez
Á Díaz-Ramos
M. Sánchez-Feutrie
X. Durán
M. Palacín
J. M. Moreno-Navarrete
Birgit Gustafson
Ann Hammarstedt
J. M. Fernández-Real
J. Vendrell
Ulf Smith
A. Zorzano
Published in Nature Cell Biology
Volume 20
Issue 4
Pages 443-454
ISSN 1465-7392
Publication year 2018
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 443-454
Language en
Links doi.org/10.1038/s41556-018-0072-9
Keywords Autophagy, Cell signalling, Fat metabolism
Subject categories Cell and Molecular Biology

Abstract

Excessive fat accumulation is a major risk factor for the development of type 2 diabetes mellitus and other common conditions, including cardiovascular disease and certain types of cancer. Here, we identify a mechanism that regulates adiposity based on the activator of autophagy TP53INP2. We report that TP53INP2 is a negative regulator of adipogenesis in human and mouse preadipocytes. In keeping with this, TP53INP2 ablation in mice caused enhanced adiposity, which was characterized by greater cellularity of subcutaneous adipose tissue and increased expression of master adipogenic genes. TP53INP2 modulates adipogenesis through autophagy-dependent sequestration of GSK3β into late endosomes. GSK3β sequestration was also dependent on ESCRT activity. As a result, TP53INP2 promotes greater β-catenin levels and induces the transcriptional activity of TCF/LEF transcription factors. These results demonstrate a link between autophagy, sequestration of GSK3β into late endosomes and inhibition of adipogenesis in vivo. © 2018 The Author(s).

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Denna text är utskriven från följande webbsida:
http://gu.se/english/research/publication/?publicationId=266502
Utskriftsdatum: 2019-10-16