The voltage-gated potassium channel KCNQ2 in Taiwanese children with febrile convulsions.

Abstract

Mutations in the voltage-gated potassium channel genes KCNQ2 and KCNQ3 have been found to cause benign familial neonatal convulsions. Recent studies provided evidence that KCNQ2 and KCNQ3 contribute to the M-current, which regulates the subthreshold electrical excitability in the CNS. Febrile convulsions represent the majority of childhood seizures, and show a strong family history, suggesting a genetic predisposition. By performing an association study, we investigated whether KCNQ2 gene polymorphisms can be used as markers of susceptibility to febrile convulsions. These data suggest that the KCNQ2 gene might not be a useful marker for prediction of the susceptibility of febrile convulsions.

• Authors: I-Ching Chou, Fuu-Jen Tsai, Chao-Ching Huang, Cheng-Chieh Lin, Chang-Hai Tsai
• Journal: Neuroreport (Neuroreport) Vol. 13 Issue 15 Pg. 1971-3 (Oct 28 2002) ISSN: 0959-4965 [Print] England
• PMID: 12395102 (Publication Type: Journal Article)

Chemical References

• Genetic Markers
• KCNQ2 Potassium Channel
• KCNQ2 protein, human
• Potassium Channels
• Potassium Channels, Voltage-Gated

Topics

• Child
• DNA Mutational Analysis
• Gene Frequency (genetics)
• Genetic Markers (genetics)
• Genetic Predisposition to Disease (genetics)
• Genetic Testing
• Genotype
• Humans
• KCNQ2 Potassium Channel
• Mutation (genetics)
• Polymorphism, Genetic (genetics)
• Potassium Channels (genetics)
• Potassium Channels, Voltage-Gated
• Seizures, Febrile (genetics, metabolism, physiopathology)
• Taiwan