TRPC channels are necessary mediators of pathologic cardiac hypertrophy

Proceedings of the National Academy of Sciences of the United States of America

Volumn 107, Issue 15, 2010, Pages 7000-7005

  Wu, Xu ^a   Eder, Petra ^a   Chang, Baojun ^a   Molkentin, Jeffery D ^a,b  

^a UNIVERSITY OF CINCINNATI   (United States)

^b HOWARD HUGHES MEDICAL INSTITUTE   (United States)

Author keywords

Calcineurin; Calcium; Heart; Signaling

Indexed keywords

CALCINEURIN; CALCIUM CHANNEL BLOCKING AGENT; CALCIUM ION; SKF 96265; TRANSCRIPTION FACTOR NFAT; TRANSIENT RECEPTOR POTENTIAL CHANNEL 1; TRANSIENT RECEPTOR POTENTIAL CHANNEL 3; TRANSIENT RECEPTOR POTENTIAL CHANNEL 4; TRANSIENT RECEPTOR POTENTIAL CHANNEL 5; TRANSIENT RECEPTOR POTENTIAL CHANNEL 6; TRANSIENT RECEPTOR POTENTIAL CHANNEL C; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; BIOLOGICAL ACTIVITY; CALCIUM TRANSPORT; COMPETITIVE INHIBITION; CONTROLLED STUDY; HEART MUSCLE CAPILLARY; HEART PERFORMANCE; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE PRESSURE; MOUSE; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEPLETION; PROTEIN EXPRESSION; RAT; SIGNAL TRANSDUCTION; STIMULATION; TRANSGENIC MOUSE;

ANIMALS; CALCINEURIN; CARDIOMEGALY; ECHOCARDIOGRAPHY; GENES, DOMINANT; MICE; MICE, TRANSGENIC; MYOCYTES, CARDIAC; NFATC TRANSCRIPTION FACTORS; PROMOTER REGIONS, GENETIC; SIGNAL TRANSDUCTION; TRANSIENT RECEPTOR POTENTIAL CHANNELS; TRPC CATION CHANNELS;

MUS MUSCULUS;

EID: 77951071535     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1001825107     Document Type: Article

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