机译:艰难梭菌毒素A通过p38,IKK和NF-κB信号通路促进树突状细胞成熟和趋化因子CXCL2表达
Department of Microbiology Hanyang University College of Medicine 17 Haengdang-dong Sungdong-gu Seoul 133-791 South Korea;
Department of Microbiology Hanyang University College of Medicine 17 Haengdang-dong Sungdong-gu Seoul 133-791 South Korea;
Department of Microbiology Hanyang University College of Medicine 17 Haengdang-dong Sungdong-gu Seoul 133-791 South Korea;
Department of Microbiology Hanyang University College of Medicine 17 Haengdang-dong Sungdong-gu Seoul 133-791 South Korea;
Department of Biotechnology Joongbu University Geumsan Choongnam 312-702 South Korea;
Department of Biomedical Engineering Hanyang University College of Medicine Seoul 133-791 South Korea;
Department of Microbiology Hanyang University College of Medicine 17 Haengdang-dong Sungdong-gu Seoul 133-791 South Korea;
Clostridium difficile toxin A; Dendritic cells; Maturation; CXCL2; Mitogen-activated protein kinase;
机译:艰难梭菌毒素A通过p38,IKK和NF-κB信号通路促进树突状细胞成熟和趋化因子CXCL2表达。
机译:NF-κB激活途径对于艰难梭菌毒素A刺激的肠上皮细胞中趋化因子表达至关重要。
机译:Clostridium Temficile毒素B通过Trim46 / Dusp1 / Mapks和NF-κB信号通路诱导结肠炎症
机译:使用X机器调查NF-κB信号传导途径中的IKK动态
机译:靶向艰难梭菌毒素A / B的肽抑制剂的开发以及表征推定的负调节剂TcdC在艰难梭菌毒素基因表达中的调节作用。
机译:IL-17A通过p38 /NF-κB信号通路协调激活MMPs表达从而促进宫颈癌细胞的迁移和侵袭性。
机译:IL-17a通过p38 / NF-κB信号通路协同激活mmps表达,促进宫颈癌细胞的迁移和侵袭。