Extracellular S100A1 Protein Inhibits Apoptosis in Ventricular Cardiomyocytes via Activation of the Extracellular Signal-regulated Protein Kinase 1/2 (ERK1/2)

Journal of Biological Chemistry

Volumn 278, Issue 48, 2003, Pages 48404-48412

  Most, Patrick ^a   Boerries, Melanie ^b   Eicher, Carmen ^a   Schweda, Christopher ^a   Ehlermann, Philipp ^a   Pleger, Sven T ^a   Loeffler, Eva ^a   Koch, Walter J ^c   Katus, Hugo A ^a   Schoenenberger, Cora Ann ^b   Remppis, Andrew ^a  

^a UNIVERSITY OF HEIDELBERG   (Germany)

^b UNIVERSITY OF BASEL   (Switzerland)

^c DUKE UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CARDIOLOGY; OXIDATION; PROTEINS; STRESSES;

APOPTOSIS;

BIOCHEMISTRY;

CALCIUM BINDING PROTEIN; CALCIUM CHANNEL L TYPE; CALCIUM ION; CLATHRIN; CYCLIC AMP DEPENDENT PROTEIN KINASE; DEOXYGLUCOSE; MITOGEN ACTIVATED PROTEIN KINASE 1; PHOSPHOLIPASE C; PROTEIN KINASE C; PROTEIN S 100; PROTEIN S 100A1; UNCLASSIFIED DRUG;

ANIMAL CELL; APOPTOSIS; ARTICLE; CALCIUM TRANSPORT; CELL SURVIVAL; ENDOCYTOSIS; ENDOSOME; ENZYME ACTIVATION; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; HEART PROTECTION; HUMAN; MOUSE; NEWBORN; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN SECRETION; SIGNAL TRANSDUCTION;

ANIMALS; ANIMALS, NEWBORN; ANTIMETABOLITES; APOPTOSIS; BLOTTING, WESTERN; CALCIUM; CALCIUM-BINDING PROTEINS; CELLS, CULTURED; CLATHRIN; CYCLIC AMP-DEPENDENT PROTEIN KINASES; DEOXYGLUCOSE; DOSE-RESPONSE RELATIONSHIP, DRUG; ENDOCYTOSIS; ENZYME ACTIVATION; FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT; HUMANS; MAP KINASE SIGNALING SYSTEM; MICROSCOPY, PHASE-CONTRAST; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; MITOGEN-ACTIVATED PROTEIN KINASES; MODELS, BIOLOGICAL; MYOCARDIUM; MYOCYTES, CARDIAC; OXIDATIVE STRESS; PHOSPHOLIPASE C; PHOSPHORYLATION; PROTEIN BINDING; PROTEIN KINASE C; S100 PROTEINS; SIGNAL TRANSDUCTION; TETRAZOLIUM SALTS; THIAZOLES; TRYPAN BLUE;

ANIMALIA;

EID: 10744225988     PISSN: 00219258     EISSN: None     Source Type: Journal    
DOI: 10.1074/jbc.M308587200     Document Type: Article

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