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

Hansson, Ola LU ; Zhou, Yuedan LU ; Renström, Erik LU and Osmark, Peter LU (2010) In Current Diabetes Reports 10. p.444-451
Abstract
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.... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Current Diabetes Reports
volume
10
pages
444 - 451
publisher
Current Science inc.
external identifiers
  • wos:000288495200006
  • pmid:20878273
  • scopus:77958468040
ISSN
1539-0829
DOI
10.1007/s11892-010-0149-8
language
English
LU publication?
yes
id
0dae320b-e633-40ab-b923-47ec8280d5d9 (old id 1687670)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20878273?dopt=Abstract
date added to LUP
2010-10-07 15:38:27
date last changed
2018-05-29 12:30:13
@article{0dae320b-e633-40ab-b923-47ec8280d5d9,
  abstract     = {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.},
  author       = {Hansson, Ola and Zhou, Yuedan and Renström, Erik and Osmark, Peter},
  issn         = {1539-0829},
  language     = {eng},
  pages        = {444--451},
  publisher    = {Current Science inc.},
  series       = {Current Diabetes Reports},
  title        = {Molecular Function of TCF7L2: Consequences of TCF7L2 Splicing for Molecular Function and Risk for Type 2 Diabetes.},
  url          = {http://dx.doi.org/10.1007/s11892-010-0149-8},
  volume       = {10},
  year         = {2010},
}