Potentiation of B2 receptor signaling by AltB2R, a newly identified alternative protein encoded in the human bradykinin B2 receptor gene.
Alternative Splicing
/ genetics
Bradykinin
/ genetics
Endocytosis
/ genetics
Endosomes
/ genetics
HEK293 Cells
HeLa Cells
Humans
MAP Kinase Signaling System
/ genetics
Open Reading Frames
/ genetics
Protein Isoforms
/ genetics
Proteomics
Receptor, Bradykinin B2
/ genetics
Signal Transduction
/ genetics
B2 receptor (B2R)
G-protein-coupled receptors (GPCRs)
alternative open reading frames (AltORFs)
bradykinin (BK)
coding DNA sequence (CDS)
mitogen-activated protein kinases (MAPK)
signal transduction
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
Historique:
received:
19
05
2020
revised:
12
01
2021
accepted:
21
01
2021
pubmed:
27
1
2021
medline:
27
8
2021
entrez:
26
1
2021
Statut:
ppublish
Résumé
Recent functional and proteomic studies in eukaryotes (www.openprot.org) predict the translation of alternative open reading frames (AltORFs) in mature G-protein-coupled receptor (GPCR) mRNAs, including that of bradykinin B2 receptor (B2R). Our main objective was to determine the implication of a newly discovered AltORF resulting protein, termed AltB2R, in the known signaling properties of B2R using complementary methodological approaches. When ectopically expressed in HeLa cells, AltB2R presented predominant punctate cytoplasmic/perinuclear distribution and apparent cointeraction with B2R at plasma and endosomal/vesicular membranes. The presence of AltB2R increases intracellular [Ca
Identifiants
pubmed: 33497625
pii: S0021-9258(21)00100-9
doi: 10.1016/j.jbc.2021.100329
pmc: PMC7949122
pii:
doi:
Substances chimiques
Protein Isoforms
0
Receptor, Bradykinin B2
0
Bradykinin
S8TIM42R2W
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
100329Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article
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