Abstract
The transcriptional repressor RE1 silencer transcription factor (REST) is an important factor that restricts some neuronal traits to neurons. Since these traits are also present in pancreatic beta-cells, we evaluated their role by generating a model of insulin-secreting cells that express REST. The presence of REST led to a decrease in expression of its known target genes, whereas insulin expression and its cellular content were conserved. As a consequence of REST expression, the capacity to secrete insulin in response to mitochondrial fuels, a particularity of mature beta-cells, was impaired. These data provide evidence that REST target genes are required for an appropriate glucose-induced insulin secretion.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Blotting, Northern
-
Cell Line
-
Co-Repressor Proteins
-
Coloring Agents / pharmacology
-
DNA, Complementary / metabolism
-
DNA-Binding Proteins / metabolism*
-
Glucose / metabolism*
-
Insulin / metabolism*
-
Insulin Secretion
-
Islets of Langerhans / metabolism
-
Mice
-
Nerve Tissue Proteins / metabolism*
-
Neurons / metabolism*
-
Potassium Chloride / pharmacology
-
Promoter Regions, Genetic
-
RNA / metabolism
-
RNA, Messenger / metabolism
-
Repressor Proteins / metabolism*
-
Tetrazolium Salts / pharmacology
-
Thiazoles / pharmacology
-
Time Factors
-
Transcription, Genetic
-
Transfection
Substances
-
Co-Repressor Proteins
-
Coloring Agents
-
DNA, Complementary
-
DNA-Binding Proteins
-
Insulin
-
Nerve Tissue Proteins
-
RNA, Messenger
-
Rcor2 protein, mouse
-
Repressor Proteins
-
Tetrazolium Salts
-
Thiazoles
-
RNA
-
Potassium Chloride
-
thiazolyl blue
-
Glucose