Arrhythmogenesis in Timothy Syndrome is associated with defects in Ca2+-dependent inactivation

Nature Communications

Volumn 7, Issue , 2016, Pages

  Dick, Ivy E ^a   Joshi Mukherjee, Rosy ^a   Yang, Wanjun ^a   Yue, David T ^a  

^a JOHNS HOPKINS UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM CHANNEL; CALCIUM V 1.2 CHANNEL; UNCLASSIFIED DRUG; CALCIUM; CALCIUM CHANNEL L TYPE; L-TYPE CALCIUM CHANNEL ALPHA(1C);

CALCIUM; MUTATION; NERVOUS SYSTEM DISORDER; NUMERICAL MODEL; PIG;

ADULT; ANIMAL CELL; ARRHYTHMOGENESIS; ARTICLE; CALCIUM DEPENDENT INACTIVATION; CALCIUM TRANSPORT; DEPOLARIZATION; DISEASE COURSE; EXPERIMENTAL GUINEA PIG; HEART ARRHYTHMIA; HUMAN; MISSENSE MUTATION; MUSCLE CELL; NONHUMAN; POTENTIAL DIFFERENCE; SYNDROME; SYSTEMIC DISEASE; TIMOTHY SYNDROME; WHOLE CELL PATCH CLAMP; ANIMAL; AUTISM; CARDIAC MUSCLE CELL; FEMALE; GENETICS; GUINEA PIG; LONG QT SYNDROME; MALE; METABOLISM; SYNDACTYLY;

CAVIA; PHLEUM PRATENSE;

ANIMALS; ARRHYTHMIAS, CARDIAC; AUTISTIC DISORDER; CALCIUM; CALCIUM CHANNELS, L-TYPE; FEMALE; GUINEA PIGS; HUMANS; LONG QT SYNDROME; MALE; MUTATION, MISSENSE; MYOCYTES, CARDIAC; SYNDACTYLY;

EID: 84956601375     PISSN: None     EISSN: 20411723     Source Type: Journal    
DOI: 10.1038/ncomms10370     Document Type: Article

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