Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect

Molecular and Cellular Biochemistry

Volumn 374, Issue 1-2, 2013, Pages 29-36

  Yang, Xinying ^a,c   Zhang, Guojian ^b   Tang, Xuelian ^a,d   Jiao, Jieying ^b   Kim, Sung Yeon ^e   Lee, Joo Young ^f   Zhu, Tianjiao ^b   Li, Dehai ^b   Yun, Yong Gab ^e   Gu, Qianqun ^b   Park, Hyun ^a  

^a Wonkwang University School of Medicine   (South Korea)

^b OCEAN UNIVERSITY OF CHINA   (China)

^c SHANGHAI INSTITUTE OF MATERIA MEDICA   (China)

^d SOUTH CHINA AGRICULTURAL UNIVERSITY   (China)

^e Wonkwang University   (South Korea)

^f Gwangju Institute of Science and Technology (GIST)   (South Korea)

Author keywords

ACTG toxin H; LPS; TLR4 NF B

Indexed keywords

ACTG TOXIN H; ANTIINFLAMMATORY AGENT; CYCLOOXYGENASE 2; DNA; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INDUCIBLE NITRIC OXIDE SYNTHASE; INTERLEUKIN 1BETA; LIPOPOLYSACCHARIDE; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE P38; MYELOID DIFFERENTIATION FACTOR 88; NATURAL PRODUCT; NITRIC OXIDE; PROTEIN KINASE B; TOLL LIKE RECEPTOR 4; UNCLASSIFIED DRUG;

ALTERNARIA ALTERNATA; ANIMAL CELL; ANTIINFLAMMATORY ACTIVITY; ARTICLE; CELL STRAIN HEK293; CELL VIABILITY; CONTROLLED STUDY; CYTOKINE PRODUCTION; DRUG MECHANISM; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; ENZYME SYNTHESIS; GEL MOBILITY SHIFT ASSAY; GENE EXPRESSION; GENETIC TRANSFECTION; MOUSE; NONHUMAN; PROMOTER REGION; PROTEIN DNA BINDING; PROTEIN EXPRESSION;

ALTERNARIA; ANIMALS; ANTI-INFLAMMATORY AGENTS; CELL LINE; CELL SURVIVAL; CYCLOOXYGENASE 2; DNA-BINDING PROTEINS; ENZYME ACTIVATION; HEK293 CELLS; HUMANS; INFLAMMATION; INTERLEUKIN-1BETA; INTERLEUKIN-6; LIPOPOLYSACCHARIDES; MACROPHAGES; MICE; MYCOTOXINS; NF-KAPPA B; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE II; P38 MITOGEN-ACTIVATED PROTEIN KINASES; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TOLL-LIKE RECEPTOR 4;

ALTERNARIA;

EID: 84871960757     PISSN: 03008177     EISSN: 15734919     Source Type: Journal    
DOI: 10.1007/s11010-012-1502-9     Document Type: Article

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