Abstract
Carbohydrate responsive element-binding protein (ChREBP) is a transcription factor whose expression and activity are increased in pancreatic β-cells maintained at elevated glucose concentrations. We show here that ChREBP inactivation in clonal pancreatic MIN6 β-cells results in an increase in Pdx-1 expression at low glucose and to a small, but significant, increase in Ins2, GcK and MafA gene expression at high glucose concentrations. Conversely, adenovirus-mediated over-expression of ChREBP in mouse pancreatic islets results in decreases in Pdx-1, MafA, Ins1, Ins2 and GcK mRNA levels. These data suggest that strategies to reduce ChREBP activity might protect against β-cell dysfunction in type 2 diabetes.
| Original language | English |
|---|---|
| Pages (from-to) | 252-257 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 402 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 12 Nov 2010 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Animals
- Base Sequence
- Cell Line, Tumor
- Gene Expression Regulation
- Gene Silencing
- Glucose/metabolism
- Homeodomain Proteins/genetics
- Insulin-Secreting Cells/drug effects
- Mice
- Molecular Sequence Data
- Nuclear Proteins/genetics
- Trans-Activators/genetics
- Transcription Factors/genetics
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