Characterizations of a loss-of-function mutation in the Kir3.4 channel subunit

Biochemical and Biophysical Research Communications

Volumn 364, Issue 4, 2007, Pages 889-895

  Calloe, Kirstine ^a   Ravn, Lasse Steen ^c   Schmitt, Nicole ^a   Sui, Jin Liang ^b   Duno, Morten ^c   Haunso, Stig ^c   Grunnet, Morten ^d   Svendsen, Jesper Hastrup ^c   Olesen, Soren Peter ^a  

^a UNIVERSITY OF COPENHAGEN   (Denmark)

^b Department of Preclinical Development and Formulations   (United States)

^c Mental Health Center Glostrup   (Denmark)

^d NEUROSEARCH A S   (Denmark)

Author keywords

Arrhythmia; Atrial fibrillation; G ; GIRK; IKACh; Kir3.4

Indexed keywords

KIR3.4 CHANNEL PROTEIN; MUSCARINIC RECEPTOR; POTASSIUM CHANNEL; PROTEIN SUBUNIT; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; CONTROLLED STUDY; HEART ATRIUM FIBRILLATION; NONHUMAN; NUCLEOTIDE SEQUENCE; OOCYTE; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN EXPRESSION; VOLTAGE CLAMP; WILD TYPE; XENOPUS LAEVIS;

ANIMALS; ATRIAL FIBRILLATION; G PROTEIN-COUPLED INWARDLY-RECTIFYING POTASSIUM CHANNELS; HUMANS; ION CHANNEL GATING; MUTAGENESIS, SITE-DIRECTED; MUTATION; OOCYTES; POTASSIUM; STRUCTURE-ACTIVITY RELATIONSHIP; XENOPUS LAEVIS;

XENOPUS LAEVIS;

EID: 36148968073     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2007.10.106     Document Type: Article

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