Expression of GAD67 and novel GAD67 splice variants during human fetal pancreas development: GAD67 expression in the fetal pancreas

Esther Korpershoek, Aart M. Verwest, Ynske Ijzendoorn, Robbert Rottier, Hemmo A. Drexhage, Ronald R. De Krijger

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

Abstract

Glutamic acid decarboxylase (GAD) is a major inhibitory neurotransmitter in the brain, which catalyses the reaction of L: -glutamate to γ-aminobutyric acid. There are two isoforms of GAD, a 65-kDa form and a 67-kDa form, which are encoded by two different genes. As previous studies suggested a role for GAD67 splice variants during fetal pancreas development, we have investigated the mRNA expression of GAD67 and GAD67 splice variants in a series of 14 human fetal pancreases between 14 weeks gestation and term and in adult control pancreases by RT-PCR. In this study, we demonstrate mRNA expression of GAD67 and four GAD67 splice variants, including GAD25, in human fetal and adult specimens. Some of the splice variants, including various proportions of exon 7 or a new exon between exons 6 and 7, have not been described before in the human pancreas. We speculate that the expression of these GAD67 splice variants might be related to human fetal pancreas development.

Original languageEnglish
Pages (from-to)31-36
Number of pages6
JournalEndocrine Pathology
Volume18
Issue number1
DOIs
Publication statusPublished - Mar 2007
Externally publishedYes

Keywords

  • Fetal development
  • GAD
  • Human development
  • Pancreas alternative splicing

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