Down-regulation of miR-1/miR-133 contributes to re-expression of pacemaker channel genes HCN2 and HCN4 in hypertrophic heart

Journal of Biological Chemistry

Volumn 283, Issue 29, 2008, Pages 20045-20052

  Luo, Xiaobin ^a,b   Lin, Huixian ^a   Pan, Zhengwei ^c   Xiao, Jiening ^a   Zhang, Yong ^c   Lu, Yanjie ^c   Yang, Baofeng ^c   Wang, Zhiguo ^a,c  

^a MONTREAL HEART INSTITUTE   (Canada)

^b UNIVERSITÉ DE MONTRÉAL   (Canada)

^c HARBIN MEDICAL UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

NUCLEIC ACIDS; PATHOLOGY; RNA;

CARDIAC HYPERTROPHIES; CARDIOMYOCYTES; CELLULAR FUNCTIONS; ELECTRICAL REMODELING; FORCED EXPRESSIONS; HYPERPOLARIZATION; LEFT VENTRICULAR HYPERTROPHIES; OVEREXPRESSION; PROTEIN LEVELS; RAT MODELS; RNA INTERFERENCES; TRANSCRIPTIONAL REGULATIONS; VENTRICULAR CELLS;

GENES;

ANGIOTENSIN II; CELL MEMBRANE PROTEIN; CYCLIC NUCLEOTIDE GATED CHANNEL; MICRORNA; MIR 1; MIR 133; RNA; UNCLASSIFIED DRUG; HCN2 POTASSIUM CHANNEL; HCN4 PROTEIN, HUMAN; HCN4 PROTEIN, RAT; ION CHANNEL; MUSCLE PROTEIN; POTASSIUM CHANNEL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARRHYTHMOGENESIS; ARTICLE; CONTROLLED STUDY; DOWN REGULATION; GENE; GENE EXPRESSION; GENE EXPRESSION REGULATION; GENE HCN2; GENE HCN4; GENE OVEREXPRESSION; GENE REPRESSION; GENE SILENCING; GENE TARGETING; GENETIC TRANSCRIPTION; GENETIC TRANSFECTION; HEART AUTOMATICITY; HEART HYPERTROPHY; HEART LEFT VENTRICLE HYPERTROPHY; HEART MUSCLE CELL; HEART VENTRICLE REMODELING; HUMAN; HUMAN CELL; MALE; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; RAT; RNA INTERFERENCE; TISSUE LEVEL; UPREGULATION; ANIMAL; CARDIOMEGALY; CELL CULTURE; GENETICS; HEART VENTRICLE; METABOLISM; NUCLEOTIDE SEQUENCE; SPRAGUE DAWLEY RAT;

RATTUS;

ANIMALS; ANIMALS, NEWBORN; BASE SEQUENCE; CARDIOMEGALY; CELLS, CULTURED; CYCLIC NUCLEOTIDE-GATED CATION CHANNELS; DOWN-REGULATION; HEART VENTRICLES; ION CHANNELS; MALE; MICRORNAS; MUSCLE PROTEINS; POTASSIUM CHANNELS; RATS; RATS, SPRAGUE-DAWLEY;

EID: 50649111705     PISSN: 00219258     EISSN: 1083351X     Source Type: Journal    
DOI: 10.1074/jbc.M801035200     Document Type: Article

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