Endogenous activated protein C signaling is critical to protection of mice from lipopolysaccaride-induced septic shock

Journal of Thrombosis and Haemostasis

Volumn 7, Issue 5, 2009, Pages 851-856

  Xu, J ^a   Ji, Y ^a   Zhang, X ^b   Drake, M ^b   Esmon, Charles T ^a,b,c  

^a OKLAHOMA MEDICAL RESEARCH FOUNDATION   (United States)

^b UNIVERSITY OF OKLAHOMA HEALTH SCIENCES CENTER   (United States)

^c UNIVERSITY OF OKLAHOMA COLLEGE OF MEDICINE   (United States)

Author keywords

Activated protein C; Anticoagulation; Cytoprotection; Sepsis

Indexed keywords

ACTIVATED PROTEIN C; BACTERIUM LIPOPOLYSACCHARIDE; CREATININE; INTERLEUKIN 6; MONOCLONAL ANTIBODY; NITROGEN; UREA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANTICOAGULATION; ARTICLE; CELL MEMBRANE PERMEABILITY; CELL PROTECTION; CONTROLLED STUDY; CREATININE BLOOD LEVEL; CYTOKINE RELEASE; IMMUNOCHEMISTRY; INHIBITION KINETICS; KIDNEY FAILURE; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN BINDING; PROTEIN FUNCTION; SEPTIC SHOCK; SIGNAL TRANSDUCTION; SURVIVAL; UREA NITROGEN BLOOD LEVEL;

ANIMALS; ANTIBODIES, MONOCLONAL; BLOOD UREA NITROGEN; CELL LINE; CREATININE; INTERLEUKIN-6; LIPOPOLYSACCHARIDES; MALE; MICE; MICE, INBRED C57BL; PROTEIN C; SHOCK, SEPTIC; SIGNAL TRANSDUCTION;

EID: 65349138302     PISSN: 15387933     EISSN: 15387836     Source Type: Journal    
DOI: 10.1111/j.1538-7836.2009.03333.x     Document Type: Article

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