Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers susceptibility to hyperoxic lung injury in mice

American Journal of Physiology - Lung Cellular and Molecular Physiology

Volumn 285, Issue 1 29-1, 2003, Pages

  Morse, Danielle ^a   Otterbein, Leo E ^a   Watkins, Simon ^a   Alber, Sean ^a   Zhou, Zhihong ^a   Flavell, Richard A ^b   Davis, Roger J ^c   Choi, Augustine M K ^a,d  

^a UNIVERSITY OF PITTSBURGH SCHOOL OF MEDICINE   (United States)

^b YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL   (United States)

^d UNIVERSITY OF PITTSBURGH   (United States)

Author keywords

Apoptosis; Hyperoxia; Mitogen activated protein kinase; Oxidative stress; Oxygen toxicity; Stress response

Indexed keywords

HEME OXYGENASE 1; LIPOPOLYSACCHARIDE; MITOGEN ACTIVATED PROTEIN KINASE; MYELOPEROXIDASE; STRESS ACTIVATED PROTEIN KINASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; DISEASE PREDISPOSITION; ENZYME DEFICIENCY; HYPEROXIA; LUNG INJURY; LUNG LAVAGE; MALE; MOUSE; NICK END LABELING; NONHUMAN; OXIDATIVE STRESS; OXYGEN TOXICITY; PATHOPHYSIOLOGY; PRIORITY JOURNAL;

EID: 0037974646     PISSN: 10400605     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajplung.00387.2002     Document Type: Article

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