Second Department of Internal Medicine, Asahikawa Medical College, Nishikagura, Asahikawa,Japan;
Department of Biochemistry, Saitama Cancer Center Research Institute, Saitama, Japan;
Second Department of Internal Medicine, Asahikawa Medical College, Nishikagura, Asahikawa,Japan Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet,Stockholm, Sweden;
Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet,Stockholm, Sweden;
Second Department of Internal Medicine, Asahikawa Medical College, Nishikagura, Asahikawa,Japan Division of Clinical Immunology, ACRC, Institute of Medical Science,University of Tokyo, Tokyo, Japan;
机译:人单核细胞和巨噬细胞中的芳烃受体/二恶英受体
机译:活化的甲状腺激素受体调节人肝细胞中的二恶英诱导芳基烃受体介导的CYP1A1诱导,但不在人肝癌HepG2细胞中
机译:嵌合的芳基碳氢化合物受体基因敲除小鼠模型表明,造血细胞中的芳基碳氢化合物受体激活促进了由2,3,7,8-四氯二苯并-p-二恶英诱导的肝损伤。
机译:使用表达重组芳基烃受体基因的转基因拟南芥植物的二恶英和二恶英样化合物的高通量生物测定
机译:2,3,7,8 Tetra chlorodibenzo-p-dioxin(TCDD)的芳烃受体信号的激活改变造血干/祖细胞的细胞功能和通路特异性基因调节。
机译:在表皮等效模型中由2378-四氯二苯并-对-二恶英(TCDD)诱导的并四苯并表型取决于芳基烃受体的活化而不是由芳基烃受体的敲除而复制的
机译:2,3,7,8-四氯二苯并-对-二恶英(TCDD)在表皮等效模型中诱导并四氯苯酚表型取决于芳基烃受体的活化,而不是由芳基烃受体的敲除复制的