Gain of function mutants: Ion channels and G protein-coupled receptors

Annual Review of Neuroscience

Volumn 23, Issue , 2000, Pages 89-125

  Lester, Henry A ^a   Karschin, Andreas ^b  

^a CALIFORNIA INSTITUTE OF TECHNOLOGY   (United States)

^b MAX PLANCK INSTITUTE FOR BIOPHYSICAL CHEMISTRY   (Germany)

Author keywords

Epilepsy; Genetic disease; Long QT syndrome; Neurodegeneration; Weaver

Indexed keywords

CHLORIDE CHANNEL; G PROTEIN COUPLED RECEPTOR; ION CHANNEL; POTASSIUM CHANNEL; SODIUM CHANNEL;

APOPTOSIS; CHANNEL GATING; EPILEPSY; GENE FUNCTION; GENE INACTIVATION; GENE MUTATION; LONG QT SYNDROME; MOUSE; NERVE EXCITABILITY; NONHUMAN; PRIORITY JOURNAL; REVIEW;

EID: 0034037498     PISSN: 0147006X     EISSN: None     Source Type: Book Series    
DOI: 10.1146/annurev.neuro.23.1.89     Document Type: Review

References (2)

1. Kr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 97:175-87
2. Ackerman MJ, Schroeder JJ, Berry R, Schaid DJ, Porter CJ, et al. 1998. A novel mutation in KVLQT1 is the molecular basis of inherited long QT syndrome in a near-drowning patient's family. Pediatr. Res. 44:148-53