毒素T3DB ID

T3D0073

目标BioDB ID

BE0003721

目标名称

Aryl hydrocarbon receptor

目标UniProt ID

P35869

作用机理

Chlorinated dibenzo-p-dioxins cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. This includes 2,3,7,8-tetrachlorodibenzo-p-dioxin's carcinogenicity is thought to be the result of its ability to alter the capacity of both exogenous and endogenous substances to damage the DNA by inducing CYP1A1- and CYP1A2-dependent drug-metabolizing enzymes. (L177)

参考文献

A10051 - Roberts EA, Golas CL, Okey AB: Ah receptor mediating induction of aryl hydrocarbon hydroxylase: detection in human lung by binding of 2,3,7,8-[3H]tetrachlorodibenzo-p-dioxin. Cancer Res. 1986 Jul;46(7):3739-43. (3011254) L177 - ATSDR - Agency for Toxic Substances and Disease Registry (1998). Toxicological profile for chlorinated dibenzo-p-dioxins (CDDs). U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). (http://www.atsdr.cdc.gov/toxprofiles/tp104.html)

创建于

2009-05-21 18:03:16 UTC

更新于

2014-09-04 16:10:38 UTC

目标详情