Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Erik Renström

Erik Renström

Vice-chancellor

Erik Renström

Molecular Function of TCF7L2: Consequences of TCF7L2 Splicing for Molecular Function and Risk for Type 2 Diabetes.

Author

  • Ola Hansson
  • Yuedan Zhou
  • Erik Renström
  • Peter Osmark

Summary, in English

TCF7L2 harbors the variant with the strongest effect on type 2 diabetes (T2D) identified to date, yet the molecular mechanism as to how variation in the gene increases the risk for developing T2D remains elusive. The phenotypic changes associated with the risk genotype suggest that T2D arises as a consequence of reduced islet mass and/or impaired function, and it has become clear that TCF7L2 plays an important role for several vital functions in the pancreatic islet. TCF7L2 comprises 17 exons, five of which are alternative (ie, exons 4 and 13-16). In pancreatic islets four splice variants of TCF7L2 are predominantly expressed. The regulation of these variants and the functional consequences at the protein level are still poorly understood. A clear picture of the molecular mechanism will be necessary to understand how an intronic variation in TCF7L2 can influence islet function.

Department/s

  • Genomics, Diabetes and Endocrinology
  • Diabetes - Islet Patophysiology
  • EXODIAB: Excellence in Diabetes Research in Sweden

Publishing year

2010

Language

English

Pages

444-451

Publication/Series

Current Diabetes Reports

Volume

10

Document type

Journal article

Publisher

Current Science inc.

Topic

  • Endocrinology and Diabetes

Status

Published

Research group

  • Genomics, Diabetes and Endocrinology
  • Diabetes - Islet Patophysiology

ISBN/ISSN/Other

  • ISSN: 1539-0829