Pathophysiology of KCNQ channels: Neonatal epilepsy and progressive deafness

Epilepsia

Volumn 41, Issue 8, 2000, Pages 1068-1069

  Jentsch, T J ^a   Schroeder, B C ^a   Kubisch, C ^a   Friedrich, T ^a   Stein, V ^a  

^a UNIVERSITY OF HAMBURG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; EPILEPSY; GENE DELETION; GENE MUTATION; HEARING IMPAIRMENT; HETEROZYGOTE; NEWBORN DISEASE; NONHUMAN; PATHOPHYSIOLOGY; PRIORITY JOURNAL; XENOPUS;

EID: 0033898774     PISSN: 00139580     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1528-1157.2000.tb00302.x     Document Type: Article

References (9)

1. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias
2. A potassium channel mutation in neonatal human epilepsy
3. Benign familial neonatal convulsions linked to genetic markers on chromosome 20
4. Genetic heterogeneity in benign familial neonatal convulsions: Identification of a new locus on chromosome 8q
5. A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns
6. A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family
7. + channels causes epilepsy
8. KCNQ2 and KCNQ3 potassium channel subunits: Molecular correlates of the M-channel
9. KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness