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1 and this induction involving function of the arylhydrocarbon (Ah) receptor is inhibited by the protei
2 tion of metabolic enzymes via binding to the arylhydrocarbon receptor (AhR) and the peroxisome prolif
4 ric transcription factors which includes the arylhydrocarbon receptor (AHR), hypoxia-inducible factor
6 ceptor antagonism was identified, whereas no arylhydrocarbon receptor activity or binding to the thyr
9 RNAs encoding the AhR dimerization partners, arylhydrocarbon receptor nuclear translocator (ARNT) and
10 A mutant mouse was generated in which the arylhydrocarbon receptor nuclear translocator (Arnt) gen
11 xia-inducible factor-1alpha (Hif-1alpha) and arylhydrocarbon receptor nuclear translocator (Arnt) gen
12 helix-loop-helix factor that interacts with arylhydrocarbon receptor nuclear translocator (ARNT) in
13 activation of the HIF-alpha binding partner, arylhydrocarbon receptor nuclear translocator (Arnt), bu
14 cription factor composed of HIFalpha and the arylhydrocarbon receptor nuclear translocator (ARNT/HIF1
15 ic helix-loop-helix (bHLH)-PAS protein ARNT (arylhydrocarbon receptor nuclear transporter) forms tran
17 ARNT forms heterodimeric complexes with the arylhydrocarbon receptor, HIF-1alpha, Sim and the PAS pr
18 e receptors in mammalian brain, revealing an arylhydrocarbon receptor-independent mechanism through w