Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the biological and toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dioxin-like compounds (DLC), as well as some drugs and endogenous tryptophan metabolites []. Without ligands, AHR is part of the Hsp90/XAP2 (heat shock protein 90/hepatitis B virus X-associated protein) multi-chaperone protein complex. Upon ligand binding, the receptor dissociates from the chaperone complex and translocates into the nucleus where it heterodimerises with ARNT (AHR nuclear translocator). The respective heterodimeric complex then modulates the cell's transcriptional activity by binding to specific xenobiotic response elements (XREs) in the promoters of AHR target genes [, ].
Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the biological and toxic effects of dioxin-like compounds []. Upon ligand binding, the receptor translocates into the nucleus where it heterodimerises with ARNT (AHR nuclear translocator) []. The aryl hydrocarbon receptor repressor (AHRR) competes with AHR for the binding of ARNT, and thereby repressing AHR's transcription activity [].
Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the biological and toxic effects of dioxin-like compounds []. Upon ligand binding, the receptor translocates into the nucleus where it heterodimerises with ARNT (AHR nuclear translocator) []. The aryl hydrocarbon receptor repressor (AHRR) competes with AHR for the binding of ARNT, and thereby repressing AHR's transcription activity [].
