ライフサイエンスコーパス: Ah receptor

1 ids, on expression of genes regulated by the Ah receptor.

2 n murine hepatoma cells without a functional Ah receptor.

3 presence of either the high or low affinity Ah receptor.

4 emonstrated that the nuclear protein was the Ah receptor.

5 responsible for endogenous activation of the Ah receptor.

6 inked to regulation of the aryl hydrocarbon (Ah) receptor.

7 mpounds acting through the aryl hydrocarbon (Ah) receptor.

8 to alter the steady-state levels of cellular Ah receptor, a result that leads to a dramatic induction

9 ng nuclear factor-kappaB activation, whereas Ah receptor activation by PAH affects suppression.

10 AF1/CIP1) gene that respond to TCDD-mediated Ah receptor activation independently of p53.

11 the relationship between CYP1A1 activity and Ah receptor activation we used CYP1A1-deficient mouse he

12 Ah receptor degradation, an indicator of Ah receptor activation, does not occur after chrysin tre

13 Based on the Ah receptor activation, UAB30 was tested for its ability

14 The Ah receptor (AHR) and its DNA binding partner, the Ah re

15 The Ah receptor (AhR) and the Ah receptor nuclear translocat

16 thracene (DMBA), and that DMBA activates the Ah receptor (AhR) in these cells in vitro.

17 The Ah receptor (AHR) is a ligand-activated transcription fa

18 The Ah receptor (AhR) mediates many of the toxic responses i

19 The Ah receptor (AHR) mediates the metabolic adaptation to a

20 -PAS) proteins that interact with either the Ah receptor (AHR) or the Ah receptor nuclear translocato

21 The Ah receptor (AhR), a soluble cytosolic protein, mediates

22 ARNT is also a dimeric partner for the Ah receptor (AHR), and this complex is essential in regu

23 -4'-nitroflavone (MNF), an antagonist of the Ah receptor (AhR), suggesting the possible involvement o

24 CYP1A1 in the presence of an agonist for the Ah receptor (AhR).

25 to identify proteins that interact with the Ah receptor (AhR).

26 han 30 years, the aryl hydrocarbon receptor [Ah receptor (AHR)] has been extensively scrutinized as t

27 an interaction between the aryl hydrocarbon (Ah) receptor (AHR), a ligand-activated transcription fac

28 vation function of the acidic segment of the Ah receptor (amino acids 515-583) by reconstituting AhR-

29 UGT1A1-XRE, and competition experiments with Ah receptor and Arnt antibodies demonstrated that the nu

30 een two basic helix-loop-helix proteins (the Ah receptor and Arnt), interaction of the heterodimer wi

31 -dihydrodiol was linked to activation of the Ah receptor and induction of CYP1A1, an event that can l

32 le are important in its interaction with the Ah receptor and subsequent CYP1A1/2 induction.

33 tion between the activation of the cytosolic Ah receptor and the c-Src- and cdc37-containing HSP90 co

34 s cytoplasmic and associates with unliganded Ah receptor and with hsp90; 2,3,7,8-tetrachlorodibenzo-p

35 ng in vitro synthesized guinea pig and mouse Ah receptors and mouse Arnt.

36 o-p-dioxin (TCDD) with the aryl hydrocarbon (AH) receptor and subsequent changes in gene expression h

37 CYP1A1/2 genes through the aryl hydrocarbon (Ah) receptor and the xenobiotic response elements.

38 oligonucleotides specific for XF1 or for the AH receptor, and prepared CAT reporter gene constructs c

39 ns for chrysin as an atypical agonist of the Ah receptor are intriguing at the molecular level, the r

40 r of the AHR signaling pathway that we named Ah-receptor associated protein 3 (ARA3).

41 e associated with delayed degradation of the Ah receptor because TCDD-initiated degradation is revers

42 ulated gene, CYP1B1, suggesting that altered Ah receptor binding to DNA does not mediate reduced CYP1

43 d that 17beta-estradiol had little effect on Ah receptor binding to its DNA-responsive element.

44 L327 led to enhanced nuclear accumulation of Ah receptor but with a reduced capacity to complement TC

45 ays confirm that chrysin is a ligand for the Ah receptor by competition with [3H]2,3,7,8-tetrachlorod

46 ted the mechanism by which activation of the Ah receptor by dioxin (TCDD) was accompanied by rapid ac

47 Knock-down of the Ah receptor by siRNA indicates that chrysin uses the Ah

48 gest a novel signaling mechanism whereby the Ah receptor can stimulate proliferation and tumorigenesi

49 Results of Ah receptor competitive binding experiments indicated th

50 sh the sequence specificities of XF1 and the AH receptor complex, both of which bind to XRE1, a xenob

51 tosolic cdc37 complex, but not the cytosolic Ah receptor complex, we could show that the action of TC

52 ents demonstrated the presence of functional Ah receptor complexes in both high and low passage cells

53 iated with the aryl hydrocarbon hydroxylase (Ah) receptor (Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1).

54 ound expressing a lower affinity form of the Ah receptor (DBA allele), transgene and murine Cyp1a1 pr

55 P1A1 and to increase excretion of oxo8Gua in Ah receptor-defective c4 mutant cells.

56 Ah receptor degradation, an indicator of Ah receptor act

57 lung, via an unknown mechanism, whereas the Ah receptor-dependent enzyme induction reduces adducts i

58 In addition to regulation by an Ah receptor-dependent mechanism, expression of many memb

59 p38 by B[a]P-7,8-dihydrodiol was shown to be Ah receptor-dependent, indicating that metabolic activat

60 Erk kinase is linked to Ah receptor expression, as demonstrated by reductions in

61 indicate that in uninduced mice, the normal Ah receptor facilitates formation of IQ/DNA adducts in l

62 , under some circumstances, compete with the AH receptor for binding to XRE1.

63 anscriptional activation while targeting the Ah receptor for degradation.

64 The dependency on the Ah receptor for the induction of CYP1A1/2 by YH439 was c

65 by BPDE-2, an event that was independent of Ah receptor function.

66 ave shown that most rat hepatic genes of the Ah receptor gene battery are regulated by glucocorticoid

67 atment, and chrysin cannot transactivate the Ah receptor in a TCDD-dependent fashion.

68 tor by siRNA indicates that chrysin uses the Ah receptor in conjunction with other factors through MA

69 ite, lipoxin A4, to bind to and activate the Ah receptor in Hepa-1 cells.

70 Support for a role of the Ah receptor in normal physiology also has been reported,

71 n of CYP1A1 by PAHs such as B[a]P through an Ah receptor-independent pathway.

72 Immunoprecipitation experiments of the Ah receptor indicate that Erk kinase activity is associa

73 ds to AhR; we have designated the protein as Ah receptor-interacting protein (AIP).

74 The Ah receptor is a ligand-activated transcription factor t

75 The Ah receptor is a ligand-dependent transcription factor t

76 interesting that the carboxyl region of the Ah receptor is associated with the transactivation regio

77 These observations reveal that the Ah receptor is involved in human UGT1A1 induction.

78 n involving function of the arylhydrocarbon (Ah) receptor is inhibited by the protein kinase C (PKC)

79 med by the lack of CYP1A1/2 induction in the Ah receptor knock-out mice (Ahr-1-) as well as in murine

80 sion, as demonstrated by reductions in total Ah receptor levels after overexpression of constitutivel

81 These changes in cellular Ah receptor levels are associated with delayed degradati

82 egnenolone-16alpha-carbonitrile (PCN) or the Ah receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (

83 Therefore, it represents a new class of Ah receptor ligand and CYP1A inducer.

84 erase activity was demonstrated by a loss of Ah receptor ligand inducibility when the XRE core region

85 either through the action of a high affinity Ah receptor ligand or by an alternative regulatory pathw

86 sults establish lipoxin A4 as a new class of Ah receptor ligand, one that differs dramatically from c

87 cells that had not been exposed to exogenous Ah receptor ligands already contained transcriptionally

88 the gene was characterized and induction by Ah receptor ligands was regionalized to bases -3338 to -

89 one that differs dramatically from classical Ah receptor ligands.

90 so inducible with aryl hydrocarbon receptor (Ah receptor) ligands such as 2,3,7,8-tetrachlodibenzo-p-

91 The neutral fraction elicited Ah-receptor mediated activity after 24 h but not after 4

92 The four fractions were examined for Ah receptor-mediated potency by use of the H4IIE-luc bio

93 iotic inducible via an aromatic hydrocarbon (Ah) receptor-mediated pathway, depending upon the tissue

94 resence of additional mechanisms, other than Ah-receptor-mediated, by which the ALDH3 gene can be dif

95 No Ah receptor message or protein was detectable in the par

96 The Ah receptor (AhR) and the Ah receptor nuclear translocator (ARNT) are capable of f

97 The Ah receptor nuclear translocator (ARNT) is the dimeric p

98 inant-negative DNA-binding-defective AhR and Ah receptor nuclear translocator (Arnt) mutants provided

99 R), a transcription factor that binds to the Ah receptor nuclear translocator (ARNT) to regulate the

100 eptor (AHR) and its DNA binding partner, the Ah receptor nuclear translocator (ARNT), are basic helix

101 act with either the Ah receptor (AHR) or the Ah receptor nuclear translocator (ARNT).

102 ceptor to the nucleus, dimerization with the Ah receptor nuclear translocator, and binding of this he

103 Ah receptor orthologs have been demonstrated to mediate

104 These results confirm that the Ah receptor plays a critical role in B[a]P-7,8-dihydrodi

105 These results show that the Ah receptor possesses interconnected intrinsic cellular

106 However, key differences in Ah receptor recognition and activation of UGT1A1 by chry

107 y and an antagonist of the aryl hydrocarbon (Ah) receptor, reduced the excretion rate of oxo8Gua.

108 In contrast with other Ah receptor regulated genes, no DNA elements or transcri

109 adiol did not alter the induction of another Ah receptor-regulated gene, CYP1B1, suggesting that alte

110 gene assays revealed the presence of several Ah receptor response-element motifs in the promoter and

111 reproductive processes or interact with the Ah receptor responsible for CYP1A activity.

112 d a transient increase in mRNA levels of the Ah receptor-responsive gene CYP1A1, which peaked at 4 h,

113 proliferative, antiapoptotic function of the Ah receptor that likely plays a role in tumor progressio

114 LD78, MIP-1beta, insulin-induced protein and AH-receptor; the second set of genes includes those invo

115 Lipoxin A4 transformed the Ah receptor to an active DRE-binding form in a concentra

116 One involves function of the Ah receptor which requires PKC protein phosphorylation t

117 ydrocarbon (AH) hydroxylases and bind to the AH receptor, which is believed to mediate toxicity.

118 s its toxic action via the aryl hydrocarbon (Ah) receptor, which induces a battery of xenobiotic-meta

119 The essential role of Ah-receptor, which mediates the induction of CYP1A1, is

120 These MEF cells express either b-1 or d-type Ah receptors, with high and low affinities for AhR agoni

121 The ARE flanks the recently identified Ah receptor xenobiotic-responsive element.