Disease-associated changes in the expression of ion channels, ion receptors, ion exchangers and Ca2+-handling proteins in heart hypertrophy

Toxicology and Applied Pharmacology

Volumn 207, Issue 3, 2005, Pages 244-256

  Zwadlo, Carolin ^a   Borlak, Jürgen ^a  

^a FRAUNHOFER INSTITUTE FOR TOXICOLOGY AND EXPERIMENTAL MEDICINE   (Germany)

Author keywords

Ca2+ handling proteins; Ion channels; Ion exchangers; Spontaneously hypertensive rats; Ventricular hypertrophy

Indexed keywords

ADENOSINE TRIPHOSPHATASE (POTASSIUM SODIUM); ADENOSINE TRIPHOSPHATE; ALPHA ACTIN; ANTIPORTER; CALCIUM CHANNEL L TYPE; CALCIUM ION; CALMODULIN; CALRETICULIN; CALSEQUESTRIN; CYTOSKELETON PROTEIN; ION CHANNEL; MYOSIN HEAVY CHAIN ALPHA; MYOSIN HEAVY CHAIN BETA; PHOSPHOLAMBAN; PLASMA MEMBRANE ADENOSINE TRIPHOSPHATASE 1; PLASMA MEMBRANE ADENOSINE TRIPHOSPHATASE 4; POTASSIUM CHANNEL; PROTEIN; RECEPTOR; RYANODINE RECEPTOR; RYANODINE RECEPTOR 2; SARCOPLASMIC RETICULUM CALCIUM ADENOSINE TRIPHOSPHATASE 2A; SARCOPLASMIC RETICULUM CALCIUM ATPASE 2A; SODIUM CALCIUM EXCHANGE PROTEIN; SODIUM CALCIUM EXCHANGE PROTEIN 1; TROPONIN T; UNCLASSIFIED DRUG; VOLTAGE GATED SODIUM CHANNEL;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BLOOD VESSEL TONE; COMPARATIVE STUDY; DISEASE ASSOCIATION; ESSENTIAL HYPERTENSION; EXPERIMENT; FORCE; GENE; GENE EXPRESSION; GENE REPRESSION; GENETIC ASSOCIATION; HEART; HEART FAILURE; HEART HYPERTROPHY; HEART LEFT VENTRICLE HYPERTROPHY; HEART RIGHT VENTRICLE; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR3.4; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.1; MALE; NONHUMAN; PROTEIN INDUCTION; RAT; REGULATORY MECHANISM; SPONTANEOUSLY HYPERTENSIVE RAT;

ANIMALS; BODY WEIGHT; CALCIUM-BINDING PROTEINS; CARDIOMEGALY; CARRIER PROTEINS; CYTOSKELETAL PROTEINS; DNA PRIMERS; DNA, COMPLEMENTARY; GENE EXPRESSION; GENETIC MARKERS; ION CHANNELS; IONS; MALE; MYOCARDIUM; ORGAN SIZE; OXIDATIVE STRESS; RATS; RATS, INBRED SHR; RATS, SPRAGUE-DAWLEY; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA;

EID: 23944453689     PISSN: 0041008X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.taap.2005.01.005     Document Type: Article

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