UGGT1 retains proinsulin in the endoplasmic reticulum in an arginine dependent manner.
Arginine
Endoplasmic
Insulin
Reticulum
UGGT1
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
30 06 2020
30 06 2020
Historique:
received:
10
04
2020
accepted:
30
04
2020
pubmed:
20
5
2020
medline:
20
1
2021
entrez:
20
5
2020
Statut:
ppublish
Résumé
We sought to clarify a pathway by which L- and dD-arginine simulate insulin secretion in mice and cell lines and obtained the following novel two findings. (1) Using affinity magnetic nanobeads technology, we identified that proinsulin is retained in the endoplasmic reticulum (ER) through UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1) when arginine availability is limited. (2) L- and d-arginine release proinsulin from UGGT1 through competition with proinsulin and promote exit of proinsulin from the ER to Golgi apparatus. The ability of arginine to release proinsulin from UGGT1 closely correlates with arginine-induced insulin secretion in several models of β cells indicating that UGGT1-proinsulin interaction regulates arginine-induced insulin secretion.
Identifiants
pubmed: 32423812
pii: S0006-291X(20)30903-7
doi: 10.1016/j.bbrc.2020.04.158
pmc: PMC7863631
mid: NIHMS1661560
pii:
doi:
Substances chimiques
Proinsulin
9035-68-1
Arginine
94ZLA3W45F
Glucosyltransferases
EC 2.4.1.-
UGGT1 protein, mouse
EC 2.4.1.-
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
668-675Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK054759
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK090490
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare no competing financial interests.
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