Genetic deletion of Fas receptors or Fas ligands does not reduce infarct size after acute global ischemia-reperfusion in isolated mouse heart

Cell Biochemistry and Biophysics

Volumn 44, Issue 1, 2006, Pages 111-117

  Tekin, Demet ^a   Xi, Lei ^b   Kukreja, Rakesh C ^b  

^a ANKARA UNIVERSITY   (Turkey)

^b VIRGINIA COMMONWEALTH UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Apoptosis; Fas ligand; Fas receptor; Gene knockout; Ischemia reperfusion; Myocardial infarction; Necrosis

Indexed keywords

FAS ANTIGEN; FAS LIGAND; FASL PROTEIN, MOUSE; LACTATE DEHYDROGENASE; MEMBRANE PROTEIN; TUMOR NECROSIS FACTOR;

ANIMAL; ARTICLE; C57BL MOUSE; CORONARY ARTERY BLOOD FLOW; GENE DELETION; GENETICS; HEART INFARCTION; HEART MUSCLE; HEART VENTRICLE FUNCTION; IN VITRO STUDY; MALE; METABOLISM; MORPHOMETRICS; MOUSE; MOUSE MUTANT; PATHOLOGY; PHYSIOLOGY; REPERFUSION INJURY;

ANIMALS; ANTIGENS, CD95; BODY WEIGHTS AND MEASURES; CORONARY CIRCULATION; FAS LIGAND PROTEIN; GENE DELETION; L-LACTATE DEHYDROGENASE; MALE; MEMBRANE GLYCOPROTEINS; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCARDIAL INFARCTION; MYOCARDIAL REPERFUSION INJURY; MYOCARDIUM; TUMOR NECROSIS FACTORS; VENTRICULAR FUNCTION;

MUS;

EID: 30744442280     PISSN: 10859195     EISSN: None     Source Type: Journal    
DOI: 10.1385/CBB:44:1:111     Document Type: Article

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