Gain-of-Function Claims for Type-2-Diabetes-Associated Coding Variants in SLC16A11 Are Not Supported by the Experimental Data
Human genetic variants inSLC16A11are associatedwith increased risk of type 2 diabetes (T2D). We pre-viously identified two distinct mechanisms throughwhich co-inherited T2D-risk coding and non-codingvariants disruptSLC16A11expression and activity,thus implicating reduced SLC16A11 function as thedise...
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| Format: | Article |
| Language: | English |
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Elsevier BV
2020
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| Online Access: | https://hdl.handle.net/1721.1/125204 |