IBD-associated G protein-coupled receptor 65 variant compromises signalling and impairs key functions involved in inflammation.
Actin remodeling
Bacterial phagocytosis
G proteins
GPR65
NLRP3 inflammasome
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
received:
23
11
2021
revised:
06
02
2022
accepted:
21
02
2022
pubmed:
27
2
2022
medline:
26
4
2022
entrez:
26
2
2022
Statut:
ppublish
Résumé
Inflammatory bowel diseases (IBD) result in chronic inflammation of the gastrointestinal tract. Genetic studies have shown that the GPR65 gene, as well as its missense coding variant, GPR65*Ile231Leu, is associated with IBD. We aimed to define the signalling and biological pathways downstream of GPR65 activation and evaluate the impact of GPR65*231Leu on these. We used HEK 293 cells stably expressing GPR65 and deficient for either Gα We confirmed that GPR65 signals via the Gα We demonstrate that GPR65 exerts its effects through Gα
Sections du résumé
BACKGROUND AND AIMS
Inflammatory bowel diseases (IBD) result in chronic inflammation of the gastrointestinal tract. Genetic studies have shown that the GPR65 gene, as well as its missense coding variant, GPR65*Ile231Leu, is associated with IBD. We aimed to define the signalling and biological pathways downstream of GPR65 activation and evaluate the impact of GPR65*231Leu on these.
METHODS
We used HEK 293 cells stably expressing GPR65 and deficient for either Gα
RESULTS
We confirmed that GPR65 signals via the Gα
CONCLUSIONS
We demonstrate that GPR65 exerts its effects through Gα
Identifiants
pubmed: 35218908
pii: S0898-6568(22)00054-7
doi: 10.1016/j.cellsig.2022.110294
pmc: PMC9536022
mid: NIHMS1836470
pii:
doi:
Substances chimiques
GPR65 protein, human
0
Inflammasomes
0
Interleukin-1beta
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Receptors, G-Protein-Coupled
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
110294Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK064869
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK062432
Pays : United States
Organisme : CIHR
ID : PJT-156298
Pays : Canada
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
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