Targeted deletion of thioredoxin-interacting protein regulates cardiac dysfunction in response to pressure overload

Circulation Research

Volumn 101, Issue 12, 2007, Pages 1328-1338

  Yoshioka, Jun ^a   Imahashi, Kenichi ^b   Gabel, Scott A ^b   Chutkow, William A ^a   Burds, Aurora A ^c   Gannon, Joseph ^a   Schulze, P Christian ^a   MacGillivray, Catherine ^a   London, Robert E ^b   Murphy, Elizabeth ^b   Lee, Richard T ^a,d  

^a HARVARD MEDICAL SCHOOL   (United States)

^b NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES   (United States)

^c MASSACHUSETTS INSTITUTE OF TECHNOLOGY   (United States)

^d NONE   (United States)

Author keywords

Cardiac hypertrophy; Glucose; Reactive oxygen species

Indexed keywords

CRE RECOMBINASE; GLUCOSE; LIPOXYGENASE; REACTIVE OXYGEN METABOLITE; THIOREDOXIN; THIOREDOXIN INTERACTING PROTEIN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ATTENUATION; COMPARATIVE STUDY; CONTROLLED STUDY; ENERGY; FEMALE; GENE DELETION; GENE TARGETING; GLOBAL CHANGE; GLUCOSE TRANSPORT; HEART; HEART DISEASE; HEART LEFT VENTRICLE; HEART LEFT VENTRICLE CONTRACTILITY; HEART MUSCLE; HEART MUSCLE CELL; HEART PERFORMANCE; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE PRESSURE; HEART VENTRICLE REMODELING; HOMEOSTASIS; KNOCKOUT MOUSE; MALE; METABOLIC REGULATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION;

ANIMALS; BLOOD PRESSURE; CARDIOMEGALY; CARRIER PROTEINS; FEMALE; GENE DELETION; GENE TARGETING; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; THIOREDOXINS; VENTRICULAR REMODELING;

EID: 37349082873     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/CIRCRESAHA.106.160515     Document Type: Article

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