Translocation of δPKC to mitochondria during cardiac reperfusion enhances superoxide anion production and induces loss in mitochondrial function

Archives of Biochemistry and Biophysics

Volumn 439, Issue 2, 2005, Pages 194-199

  Churchill, Eric N ^a   Szweda, Luke I ^a,b  

^a CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b OKLAHOMA MEDICAL RESEARCH FOUNDATION   (United States)

Author keywords

Free radical; Heart; Ischemia; Mitochondria; PKC; Reperfusion; Respiration

Indexed keywords

FREE RADICAL; HYDROGEN PEROXIDE; PROTEIN KINASE C DELTA; PROTEIN KINASE C INHIBITOR; SUPEROXIDE; ENZYME INHIBITOR; PEPTIDE; PRKCD PROTEIN, RAT; PROTEIN KINASE C;

ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; CYTOSOL; HEART MITOCHONDRION; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; MALE; MITOCHONDRIAL RESPIRATION; NONHUMAN; OXIDATION REDUCTION REACTION; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN TRANSPORT; RAT; ANIMAL; DRUG ANTAGONISM; ELECTRON TRANSPORT; IN VITRO STUDY; METABOLISM; REPERFUSION INJURY; SPRAGUE DAWLEY RAT;

ANIMALS; CYTOSOL; ELECTRON TRANSPORT; ENZYME INHIBITORS; MALE; MITOCHONDRIA, HEART; MYOCARDIAL ISCHEMIA; MYOCARDIAL REPERFUSION; MYOCARDIAL REPERFUSION INJURY; OXIDATIVE STRESS; PEPTIDES; PROTEIN KINASE C; PROTEIN KINASE C-DELTA; PROTEIN TRANSPORT; RATS; RATS, SPRAGUE-DAWLEY; SUPEROXIDES;

EID: 21544446752     PISSN: 00039861     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.abb.2005.05.007     Document Type: Article

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