Abstract
Of the many common genetic variants associated with type 2 diabetes, that in TCF7L2 remains the most studied because it has the greatest effect size. However, the mechanism by which this variant alters diabetes risk remains elusive. A new study adds another layer of complexity, suggesting that the effects of TCF7L2 are context-dependent, and highlights a novel interaction that might bias a -cell to a secretory or proliferative phenotype. This in turn might open up new avenues to the restoration of insulin secretion in people with type 2 diabetes.
Original language | English (US) |
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Pages (from-to) | 14190-14191 |
Number of pages | 2 |
Journal | Journal of Biological Chemistry |
Volume | 293 |
Issue number | 36 |
DOIs | |
State | Published - Sep 7 2018 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology