1 and this induction involving function of the arylhydrocarbon (Ah) receptor is inhibited by the protei

2 tions, most likely through activation of the arylhydrocarbon receptor (AhR) pathway.

3 ric transcription factors which includes the arylhydrocarbon receptor (AHR), hypoxia-inducible factor

4                                          The arylhydrocarbon receptor agonist 6-formylindolo[3,2-b] c

5 evels were not significantly affected by the arylhydrocarbon receptor ligand beta-naphthoflavone.

6 RNAs encoding the AhR dimerization partners, arylhydrocarbon receptor nuclear translocator (ARNT) and

7    A mutant mouse was generated in which the arylhydrocarbon receptor nuclear translocator (Arnt) gen

8 xia-inducible factor-1alpha (Hif-1alpha) and arylhydrocarbon receptor nuclear translocator (Arnt) gen

9  helix-loop-helix factor that interacts with arylhydrocarbon receptor nuclear translocator (ARNT) in

10 activation of the HIF-alpha binding partner, arylhydrocarbon receptor nuclear translocator (Arnt), bu

11 cription factor composed of HIFalpha and the arylhydrocarbon receptor nuclear translocator (ARNT/HIF1

12 ic helix-loop-helix (bHLH)-PAS protein ARNT (arylhydrocarbon receptor nuclear transporter) forms tran

13 a (hypoxia-inducible factor-1alpha) and AHR (arylhydrocarbon receptor).

14  ARNT forms heterodimeric complexes with the arylhydrocarbon receptor, HIF-1alpha, Sim and the PAS pr

15 e receptors in mammalian brain, revealing an arylhydrocarbon receptor-independent mechanism through w

16  versus related fatty acid receptors and the arylhydrocarbon receptor.

17                                          The arylhydrocarbon-receptor nuclear translocator (ARNT) is