Tandem pore domain K(+)-channel TASK-3 (KCNK9) and idiopathic absence epilepsies

Am J Med Genet. 2002 Mar 8;114(2):227-9. doi: 10.1002/ajmg.10201.

Abstract

Recently, the gene coding for the tandem pore domain K(+)-channel TASK-3 (KCNK9) has been localized to the chromosomal region 8q24. Because mutations in ion channel genes have been recognized as an important factor in the etiology of abnormal neuronal excitability, TASK-3 is an interesting candidate gene for epilepsies linked to 8q24. We therefore performed a mutation analysis of the TASK-3 gene in 65 patients with childhood and juvenile absence epilepsy. Only one silent nucleotide exchange (636C/T) was detected in exon 2 of the TASK-3 coding region. No evidence for an allelic association was found between the exon 2 polymorphism and absence epilepsy. Accordingly, genetic variation of the TASK-3 coding region does not play a major role in the etiology of idiopathic absence epilepsies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Child
  • DNA / chemistry
  • DNA / genetics
  • DNA Mutational Analysis
  • Epilepsy, Absence / genetics*
  • Humans
  • Polymorphism, Single Nucleotide
  • Polymorphism, Single-Stranded Conformational
  • Potassium Channels / genetics*
  • Potassium Channels, Tandem Pore Domain*

Substances

  • KCNK9 protein, human
  • Potassium Channels
  • Potassium Channels, Tandem Pore Domain
  • DNA