The GTPase Rab37 Participates in the Control of Insulin Exocytosis.

Détails

Ressource 1Télécharger: BIB_147E6E21A42F.P001.pdf (1922.74 [Ko])
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_147E6E21A42F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
The GTPase Rab37 Participates in the Control of Insulin Exocytosis.
Périodique
Plos One
Auteur⸱e⸱s
Ljubicic S., Bezzi P., Brajkovic S., Nesca V., Guay C., Ohbayashi N., Fukuda M., Abderrhamani A., Regazzi R.
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
8
Numéro
6
Pages
e68255
Langue
anglais
Notes
Publication types: JOURNAL ARTICLE Publication Status: epublish
Résumé
Rab37 belongs to a subclass of Rab GTPases regulating exocytosis, including also Rab3a and Rab27a. Proteomic studies indicate that Rab37 is associated with insulin-containing large dense core granules of pancreatic β-cells. In agreement with these observations, we detected Rab37 in extracts of β-cell lines and human pancreatic islets and confirmed by confocal microscopy the localization of the GTPase on insulin-containing secretory granules. We found that, as is the case for Rab3a and Rab27a, reduction of Rab37 levels by RNA interference leads to impairment in glucose-induced insulin secretion and to a decrease in the number of granules in close apposition to the plasma membrane. Pull-down experiments revealed that, despite similar functional effects, Rab37 does not interact with known Rab3a or Rab27a effectors and is likely to operate through a different mechanism. Exposure of insulin-secreting cells to proinflammatory cytokines, fatty acids or oxidized low-density lipoproteins, mimicking physiopathological conditions that favor the development of diabetes, resulted in a decrease in Rab37 expression. Our data identify Rab37 as an additional component of the machinery governing exocytosis of β-cells and suggest that impaired expression of this GTPase may contribute to defective insulin release in pre-diabetic and diabetic conditions.
Pubmed
Web of science
Open Access
Oui
Création de la notice
23/07/2013 12:28
Dernière modification de la notice
20/08/2019 12:43
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