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Type 2 Diabetes Variants Disrupt Function of SLC16A11 through Two Distinct Mechanisms.

Cell. 2017; 
Rusu Victor,Hoch Eitan,Mercader Josep M,Tenen Danielle E,Gymrek Melissa,Hartigan Christina R,DeRan Michael,von Grotthuss Marcin,Fontanillas Pierre,Spooner Alexandra,Guzman Gaelen,Deik Amy A,Pierce Kerry A,Dennis Courtney,Clish Clary B,Carr Steven A,Wagner Bridget K,Schenone Monica,Ng Maggie C Y,Chen Brian H, , ,Centeno-Cruz Federico,Zerrweck Carlos,Orozco Lorena,Altshuler David M,Schreiber Stuart L,Florez Jose C,Jacobs Suzanne B R,Lander Er
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摘要

Type 2 diabetes (T2D) affects Latinos at twice the?rate?seen in populations of European descent. We?recently identified a risk haplotype spanning SLC16A11 that explains ~20% of the increased T2D prevalence in Mexico. Here, through genetic fine-mapping, we define a set of tightly linked variants likely to contain the causal allele(s). We show that variants on the T2D-associated haplotype have two distinct effects: (1) decreasing SLC16A11 expression in liver and (2) disrupting a key interaction with basigin, thereby reducing cell-surface localization. Both independent mechanisms reduce SLC16A11 function and suggest SLC16A11 is the causal gene at?this locus. To gain insight into how SLC16A11 disruption imp... More

关键词

MCT11,SLC16A11,disease mechanism,fatty acid metabolism,genetics,lipid metabolism,monocarboxylates,precision medicine,solute carrier (SLC),type 2 diabetes (