Involvement of the MAPK and PI3K pathways in chitinase 3-like 1-regulated hyperoxia-induced airway epithelial cell death

Biochemical and Biophysical Research Communications

Volumn 421, Issue 4, 2012, Pages 790-796

  Kim, Mi Na ^a   Lee, Kyung Eun ^a   Hong, Jung Yeon ^a   Heo, Won Il ^a   Kim, Kyung Won ^a   Kim, Kyu Earn ^a   Sohn, Myung Hyun ^a  

^a Yonsei University College of Medicine   (South Korea)

Author keywords

Cell death; Chitinase 3 like 1; Human airway epithelial cell; Hyperoxia; Mitogen activated protein kinase; Phosphatidylinositol 3 kinase

Indexed keywords

CASPASE 3; CASPASE 7; CHITINASE; CHITINASE 3 LIKE 1; LIPOCORTIN 5; MITOGEN ACTIVATED PROTEIN KINASE; OXYGEN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CELL DEATH; CELL LINE; ELECTRON MICROSCOPY; HUMAN; HUMAN CELL; HYPEROXIA; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; RESPIRATORY EPITHELIUM; SIGNAL TRANSDUCTION; STAINING;

ADIPOKINES; APOPTOSIS; CELL LINE; GENE KNOCKDOWN TECHNIQUES; HUMANS; LECTINS; MAP KINASE SIGNALING SYSTEM; OXIDATIVE STRESS; OXYGEN; PHOSPHATIDYLINOSITOL 3-KINASES; RESPIRATORY MUCOSA;

MURINAE;

EID: 84861224169     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2012.04.085     Document Type: Article

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