Macroscopic properties of spontaneous mutations in slow-channel syndrome: Correlation by domain and disease severity

Synapse

Volumn 60, Issue 6, 2006, Pages 441-449

  Zayas, Roberto ^a   Lasalde Dominicci, Jose ^b   Gomez, Christopher M ^c  

^a UNIVERSITY OF MINNESOTA   (United States)

^b UNIVERSITY OF PUERTO RICO   (Puerto Rico)

^c UNIVERSITY OF CHICAGO   (United States)

Author keywords

AChR; Ca2+ permeability; Channelopathy; Desensitization; Neuromuscular; Nicotinic

Indexed keywords

ACETYLCHOLINE; CHOLINERGIC RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM TRANSPORT; CELL STRAIN HEK293; CHANNEL GATING; CONGENITAL MYASTHENIC SYNDROME; CONTROLLED STUDY; DISEASE SEVERITY; FATIGUE; GENETIC TRANSFECTION; HISTOCHEMISTRY; HUMAN; HUMAN CELL; HUMAN TISSUE; MATHEMATICAL MODEL; MISSENSE MUTATION; MOUSE; MUSCLE BIOPSY; NEUROMUSCULAR JUNCTION DISORDER; NEUROMUSCULAR TRANSMISSION; NONHUMAN; PRIORITY JOURNAL; RECEPTOR DOWN REGULATION; SPONTANEOUS MUTATION; TRANSGENIC MOUSE; WEAKNESS; WILD TYPE;

AGE OF ONSET; ALGORITHMS; CALCIUM; CELL LINE; CELL MEMBRANE PERMEABILITY; ELECTROPHYSIOLOGY; HUMANS; INFANT; MUTATION; NEUROMUSCULAR DISEASES; NEUROMUSCULAR JUNCTION; PATCH-CLAMP TECHNIQUES; PHENOTYPE; RECEPTORS, CHOLINERGIC;

EID: 33748599583     PISSN: 08874476     EISSN: 10982396     Source Type: Journal    
DOI: 10.1002/syn.20317     Document Type: Article

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