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Título del libro: Protein Homeostasis Diseases: Mechanisms And Novel Therapies
Título del capítulo: Protein homeostasis and regulation of intracellular trafficking of G protein-coupled receptors

Autores UNAM:
ALFREDO ANTONIO ULLOA Y AGUIRRE; TERESA DE JESUS ZARIÑAN GARCIA;
Autores externos:

Idioma:

Año de publicación:
2020
Palabras clave:

CELL-SURFACE EXPRESSION; PARATHYROID-HORMONE RECEPTOR; MEDIATED SIGNALING DOWNSTREAM; V2 VASOPRESSIN RECEPTORS; C-TERMINAL TAIL; BETA-ARRESTIN; ENDOPLASMIC-RETICULUM; PLASMA-MEMBRANE; QUALITY-CONTROL; WILD-TYPE


Resumen:

G protein-coupled receptors (GPCRs) regulate a countless number of cellular functions and are currently major protein targets for drug discovery, as they frequently lead to disease. Like any other protein, GPCRs must be properly folded into a mature tertiary conformation compatible with quaternary assembly and endoplasmic reticulum export to the cell surface plasma membrane. Several primary and secondary structural features, including presence of particular amino acid residues and short motifs and, in addition, posttranslational modifications (PTMs), regulate the intracellular trafficking of this class of membrane proteins. In contrast to the paucity in knowledge on the molecular mechanisms underlying GPCR cell surface delivery after biosynthesis (anterograde or upward trafficking), our understanding of the processes following internalization and endocytosis of GPCRs from the plasma membrane has almost exponentially increased during the last decade, and the function of the intracellular compartments and interacting proteins that regulate the fate of the internalized receptors, either to the degradation or recycling pathways, as well as their endosomal signaling after endocytosis, are currently under intense investigation. Knowing how GPCRs traffic within the cell is essential for continuing to pave the way in the discovery of new therapeutic strategies for an array of diseases caused by receptor misrouting. © 2020 Elsevier Inc. All rights reserved.


Entidades citadas de la UNAM: