Stathmin-2 Mediates Glucagon Secretion From Pancreatic α-Cells.
alpha cell
glucagon
glucagon hypersecretion
glucagon interactome
stathmin-2
Journal
Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782
Informations de publication
Date de publication:
2020
2020
Historique:
received:
06
11
2019
accepted:
14
01
2020
entrez:
3
3
2020
pubmed:
3
3
2020
medline:
3
3
2020
Statut:
epublish
Résumé
Inhibition of glucagon hypersecretion from pancreatic α-cells is an appealing strategy for the treatment of diabetes. Our hypothesis is that proteins that associate with glucagon within alpha cell secretory granules will regulate glucagon secretion, and may provide druggable targets for controlling abnormal glucagon secretion in diabetes. Recently, we identified a dynamic glucagon interactome within the secretory granules of the α cell line, αTC1-6, and showed that select proteins within the interactome could modulate glucagon secretion. In the present study, we show that one of these interactome proteins, the neuronal protein stathmin-2, is expressed in αTC1-6 cells and in mouse pancreatic alpha cells, and is a novel regulator of glucagon secretion. The secretion of both glucagon and Stmn2 was significantly enhanced in response to 55 mM K
Identifiants
pubmed: 32117057
doi: 10.3389/fendo.2020.00029
pmc: PMC7011091
doi:
Substances chimiques
RNA, Small Interfering
0
Stathmin
0
Stmn2 protein, mouse
0
Glucagon
9007-92-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
29Informations de copyright
Copyright © 2020 Asadi and Dhanvantari.
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