Control of Insulin Release by Transient Receptor Potential Melastatin 3 (TRPM3) Ion Channels.
Transient receptor potential M3 channels (TRPM3); Calcium; Glucose-stimulated insulin secretion; CRISPR/Cas; INS-1; Trpm3 knockout
Journal
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN: 1421-9778
Titre abrégé: Cell Physiol Biochem
Pays: Germany
ID NLM: 9113221
Informations de publication
Date de publication:
10 Nov 2020
10 Nov 2020
Historique:
accepted:
28
10
2020
entrez:
9
11
2020
pubmed:
10
11
2020
medline:
28
5
2021
Statut:
ppublish
Résumé
The release of insulin in response to increased levels of glucose in the blood strongly depends on Ca We used INS-1 cells as a beta cell model in which we analysed the occurrence of TRPM3 isoformes by immunoprecipitation and western blotting and by cloning of RT-PCR amplified cDNA fragments. We applied pharmacological as well as CRISPR/Cas9-based strategies to analyse the interplay of TRPM3 and voltage-gated Ca TRPM3 channels triggered the activity of voltage-gated Ca The present study suggests an important role for TRPM3 channels in the control of glucose-dependent insulin release.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
The release of insulin in response to increased levels of glucose in the blood strongly depends on Ca
METHODS
METHODS
We used INS-1 cells as a beta cell model in which we analysed the occurrence of TRPM3 isoformes by immunoprecipitation and western blotting and by cloning of RT-PCR amplified cDNA fragments. We applied pharmacological as well as CRISPR/Cas9-based strategies to analyse the interplay of TRPM3 and voltage-gated Ca
RESULTS
RESULTS
TRPM3 channels triggered the activity of voltage-gated Ca
CONCLUSION
CONCLUSIONS
The present study suggests an important role for TRPM3 channels in the control of glucose-dependent insulin release.
Substances chimiques
TRPM Cation Channels
0
TRPM3 protein, mouse
0
TRPM3 protein, rat
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1115-1131Subventions
Organisme : DFG (Deutsche Forschungsgemeinschaft)
ID : CRC 894 A3, CRC 894 A14, CRC 894 P2, CRC 1188 B02
Pays : Germany
Informations de copyright
© Copyright by the Author(s). Published by Cell Physiol Biochem Press.
Déclaration de conflit d'intérêts
The authors have no conflicts of interest to declare.