A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns

Nat Genet. 1998 Jan;18(1):25-9. doi: 10.1038/ng0198-25.

Abstract

Idiopathic generalized epilepsies account for about 40% of epilepsy up to age 40 and commonly have a genetic basis. One type is benign familial neonatal convulsions (BFNC), a dominantly inherited disorder of newborns. We have identified a sub-microscopic deletion of chromosome 20q13.3 that co-segregates with seizures in a BFNC family. Characterization of cDNAs spanning the deleted region identified one encoding a novel voltage-gated potassium channel, KCNQ2, which belongs to a new KQT-like class of potassium channels. Five other BFNC probands were shown to have KCNQ2 mutations, including two transmembrane missense mutations, two frameshifts and one splice-site mutation. This finding in BFNC provides additional evidence that defects in potassium channels are involved in the mammalian epilepsy phenotype.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Base Sequence
  • Cell Line, Transformed
  • Chromosome Deletion
  • Chromosomes, Human, Pair 20
  • DNA, Complementary
  • Epilepsy / genetics*
  • Female
  • Humans
  • Infant, Newborn
  • KCNQ2 Potassium Channel
  • Male
  • Molecular Sequence Data
  • Mutation*
  • Pedigree
  • Potassium Channels / genetics*
  • Potassium Channels, Voltage-Gated
  • Sequence Homology, Amino Acid

Substances

  • DNA, Complementary
  • KCNQ2 Potassium Channel
  • KCNQ2 protein, human
  • Potassium Channels
  • Potassium Channels, Voltage-Gated

Associated data

  • GENBANK/AF033348
  • GENBANK/D82346