Depalmitoylation and cell physiology: APT1 as a mediator of metabolic signals.
Am J Physiol Cell Physiol
; 326(4): C1034-C1041, 2024 Apr 01.
Article
en En
| MEDLINE
| ID: mdl-38344800
ABSTRACT
More than half of the global population is obese or overweight, especially in Western countries, and this excess adiposity disrupts normal physiology to cause chronic diseases. Diabetes, an adiposity-associated epidemic disease, affects >500 million people, and cases are projected to exceed 1 billion before 2050. Lipid excess can impact physiology through the posttranslational modification of proteins, including the reversible process of S-palmitoylation. Dynamic palmitoylation cycling requires the S-acylation of proteins by acyltransferases and the depalmitoylation of these proteins mediated in part by acyl-protein thioesterases (APTs) such as APT1. Emerging evidence points to tissue-specific roles for the depalmitoylase APT1 in maintaining homeostasis in the vasculature, pancreatic islets, and liver. These recent findings raise the possibility that APT1 substrates can be therapeutically targeted to treat the complications of metabolic diseases.
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Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Tioléster Hidrolasas
/
Lipoilación
Idioma:
En
Revista:
Am J Physiol Cell Physiol
Asunto de la revista:
FISIOLOGIA
Año:
2024
Tipo del documento:
Article