ライフサイエンスコーパス: HNF-1

1 HNF-1 alpha, GATA-4, and Cdx2 interact in vitro and in v

2 HNF-1/c-Fos and HNF-1/STAT3 protein complexes were detec

3 s via an intact hepatocyte nuclear factor 1 (HNF-1) site and was dependent on the presence of endogen

4 An element for hepatocyte nuclear factor 1 (HNF-1) was identified in the SGLT1 promoter that formed

5 cription factor hepatocyte nuclear factor-1 (HNF-1) and specifically suppresses the transcription of

6 HepG2 cells, a hepatocyte nuclear factor-1 (HNF-1) binding site was critical for the full induction

7 d the role of a hepatocyte nuclear factor-1 (HNF-1) cis-acting element to regulate SI gene expression

8 mutagenesis of the hepatic nuclear factor-1 (HNF-1) consensus motif within this domain eliminates bas

9 otein levels of hepatocyte nuclear factor-1 (HNF-1), a transcription factor that regulates sterol 27-

10 inding site for hepatocyte nuclear factor-1 (HNF-1).

11 Regulation of HNF-4/HNF-1 expression by HNF-3alpha and HNF-3beta was studied

12 encoding the liver-enriched trans activators HNF-1, HNF-4, HNF-3 alpha, and HNF-3 beta was not affect

13 show that hepatocyte nuclear factor-1 alpha (HNF-1 alpha), GATA-4, and caudal related homeodomain pro

14 ene that is highly dependent on HNF-4 alpha, HNF-1 alpha, was reduced.

15 HNF-1beta revealed that it could not bind an HNF-1 target sequence or stimulate transcription of a re

16 Transcription factors (PDX-1 and HNF-1 alpha) binding to A elements are critical regulato

17 acted with two IL-6 responsive elements, and HNF-1 alpha and HNF-3/Octamer-like factors interacted wi

18 HNF-1/c-Fos and HNF-1/STAT3 protein complexes were detected in mouse liv

19 s where GATA-4 requires the presence of both HNF-1 alpha and Cdx2.

20 Thus, we hypothesize that, in LLC-PK cells, HNF-1 is acting as an accessory factor to enhance PKA si

21 the apoM promoter and identified a conserved HNF-1 binding site.

22 d1 gene contains an evolutionarily conserved HNF-1-binding site that is located near a region of deox

23 This suggests that the DCoH1.HNF-1 complex must co-fold to interact.

24 of regeneration, including NF-kappaB, C/EBP, HNF-1, CREB, as well as factors, such as ATF, AP-2, LEF-

25 s for hepatocyte nuclear factors (especially HNF-1 and HNF-4) and CCAAT/enhancer-binding protein (C/E

26 In transfection experiments, HNF-1 alpha activated the SI promoter via the SIF3 eleme

27 t on the presence of endogenous liver factor HNF-1 and induced factors STAT3 and AP-1 (c-Fos/c-Jun).

28 of the tissue-specific transcription factor HNF-1 (hepatocyte nuclear factor-1) through binding the

29 ization cofactor of the transcription factor HNF-1.

30 well as genes for the transcription factors HNF-1, vHNF-1, and HNF-4.

31 tion of corresponding transcription factors (HNF-1, NK-kappaB, CREB, C/EBP-alpha and C/EBP-beta, GATA

32 y at least three host transcription factors: HNF-1, HNF-4, and Oct-1.

33 epatic cell lines overexpressing STAT3/c-Fos/HNF-1.

34 he regulation of pregenomic RNA in WHV, (ii) HNF-1 is essential for EnII function in vivo, and (iii)

35 ver-enriched transcription factors including HNF-1 alpha, HNF-3, HNF-4, and C/EBP beta, and the more

36 veral known transcription factors, including HNF-1 and Sp1 within the first 1 kb.

37 on from Promoter 2 is dependent on an intact HNF-1 consensus binding site which binds the transcripti

38 decline in the abundance of ovine intestinal HNF-1 and SGLT1 transcripts during transition from preru

39 sion of the nonneuronal form of AADC mRNA is HNF-1.

40 Transgenic SI gene constructs with a mutated HNF-1 element (SIF3) revealed a strong reduction in prom

41 ransactivation and DNA binding activities of HNF-1.

42 activation and the DNA binding activities of HNF-1.

43 eover, LPS decreases the binding activity of HNF-1 by 70% in nuclear extracts in hamster liver, sugge

44 27-hydroxylase by decreasing the binding of HNF-1 to its promoter.

45 an antibody to HNF-1 demonstrated binding of HNF-1 to the KL-1 fragment and cotransfection of HNF-1 c

46 ptional coactivator dimerization cofactor of HNF-1 (DCoH).

47 coactivator, DCoH (dimerization cofactor of HNF-1).

48 1 to the KL-1 fragment and cotransfection of HNF-1 cDNA into cells which do not express the nonneuron

49 plasm to a dimer interacting with a dimer of HNF-1 in the nucleus.

50 To investigate the basis for dimerization of HNF-1 proteins, we determined the 1.2 A resolution X-ray

51 We propose that exchange of HNF-1 dimerization partners contributes to circadian cha

52 r via the SIF3 element, and co-expression of HNF-1 beta impaired this transcriptional activation.

53 t TSE2-mediated extinction is independent of HNF-1, -4, -3 alpha, and -3 beta expression.

54 1alpha activation domains or interruption of HNF-1-binding sites in the lactase-phlorizin hydrolase p

55 result demonstrates that decreased levels of HNF-1 alpha per se can cause MODY.

56 iption in vivo and suggest that the ratio of HNF-1 alpha to HNF-1 beta plays a role in the transcript

57 These findings imply a combinatory role of HNF-1 alpha, Cdx2, and GATA-4 for the time- and position

58 er representative mammalian TFs (c-myc, p53, HNF-1 and CREB).

59 nduced (STAT3 and AP-1) and tissue specific (HNF-1), can interact as an adaptive response to liver in

60 These data indicate that HNF-1 plays an important role in the glucose responsiven

61 alpha-fibrinogen promoters, indicating that HNF-1/IL-6/STAT3/AP-1-mediated transactivation of hepati

62 Immunolocalization experiments revealed that HNF-1 alpha is detected in rare epithelial cells of suck

63 The HNF-1 dimerization domain forms a unique, four-helix bun

64 ent effects on the core promoter bearing the HNF-1 binding site.

65 -PK cells to the same degree as deleting the HNF-1 site.

66 dependent upon EnII, mutations in either the HNF-1 or the HNF-4 site strongly reduced CAT activity, w

67 t they are less common than mutations in the HNF-1 alpha/MODY3 gene.

68 a complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both d

69 oM promoter, that a specific mutation in the HNF-1 binding site abolished transcriptional activation

70 In transfected HepG2 cells, lesions in the HNF-1 site inactivated pregenomic RNA expression and vir

71 at, as expected, viruses with lesions in the HNF-1 site were nearly noninfectious, while mutants with

72 enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the H

73 nucleotide-58 of the promoter region of the HNF-1 alpha gene cosegregates with MODY.

74 both the promoter and coding regions of the HNF-1 alpha gene should be screened for mutations in sub

75 ndings demonstrate the essential role of the HNF-1 regulatory element to support SI gene transcriptio

76 Mutations of the HNF-1 site or expression of a dominant-negative HNF-1bet

77 mobility-shift assays, the intensity of the HNF-1-binding complex to the target promoter sequence de

78 ly, while both X and X(mt) can stimulate the HNF-1 activities, they differ in their effects: a smalle

79 stimulation of the IGFBP-1 promoter via the HNF-1 site.

80 Changing this HNF-1 motif to that for the yeast transcription factor G

81 and suggest that the ratio of HNF-1 alpha to HNF-1 beta plays a role in the transcriptional activity

82 ility shift studies utilizing an antibody to HNF-1 demonstrated binding of HNF-1 to the KL-1 fragment

83 and its mutant X(mt) can physically bind to HNF-1 both in vitro and in vivo.

84 the other hand, BSIF-3, like SIF-3, binds to HNF-1 and also represses transcription from the apoB pro

85 When HNF-1 alpha or HNF-3/Octamer-like factors were independe

86 We wanted to study whether HNF-1 alpha, GATA-4, and Cdx2 can cooperate in the regul

87 orms it will not dissociate to interact with HNF-1.

88 -4 has strong synergistic relationships with HNF-1, HNF-4 and HNF-3beta and with C/EBPbeta.