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AhR:encounter with endogenous derivatives - Coggle Diagram
AhR:encounter with endogenous derivatives
Endo and Exogenous ligands: derivatives of tryptophan such as indigo dye and indirubin, tetrapyrroles such as bilirubin, the arachidonic acid metabolites lipoxin A4 and prostaglandin G, modified low-density lipoprotein and several dietary carotenoids.
ligand binding(PAS b domain)
translocation of the ligand-receptor complex into the nucleus
dissociation of chaperons(HSP90/p23)
the complex heterodimerizes with ARNT
binding to specific DNA sequences located in the promoter regions of target genes named xenobiotic response elements (XRE, 5′-TA/TGCGTG-3′)
transcription of target genes by the recruitment of various components of the transcriptional machinery
CBP/p300 (cAMP response element-binding protein binding protein)
SRC-1 (steroid receptor coactivator 1)
p160/bHLH-PAS, NCoA2/GRIP1/TIF2 (Nuclear receptor Coactivator 2/Glucocorticoid Receptor Interacting Protein 1/Transcriptional Intermediate Factor 2)
p/CIP (p300/CBP/CoIntegrator-associated Protein
RIP140 (Receptor Interacting Protein 140)
ATP-dependent chromatin remodeling components such as BRG-1 (Brahma Related Gene)
CYP1A1,CYP1A2,CYP1B1
Cell death
AHR expression is upregulated in developing TH17
cells and involved in boosting IL-17A, IL-17F and
IL-22 production
AHR limits STAT5 and STAT1,known to interfere with TH17 cell
cooperates with STAT3
to induce expression of the transcription factor aiolos
silecing IL-2
facilitates the recruitment of RORγt to the Il22
promoter
mediates the conversion of TH17 cells into IL-10-producing
anti-inflammatory TR1 cells
ITE(AHR agonist) inhibits TH17 differetion in allergic rhinitis while favouring IL-10 production by Treg cells
coal tar
AHR activation
epidermal differentiation
restored expression of major skin barrier
proteins, including filaggrin
interfering with STAT6
tapinarf
AHR activation
moderates
proinflammatory cytokine expression
used experiment for AHR mechanism
siRNA
AHR deficient mice
AhR KO mice
AHR activation by agonists, in cigarette smoke worsens experimental autoimmunity, by enhancing pathogenic TH17 cell generation9
NPD-0614-13 and NPD-0614-24