ライフサイエンスコーパス: HNF

1 HNF-1alpha-mutated lesions could be distinguished from o

2 HNF-1alpha-mutated lesions had the lowest lesion signal

3 HNF-1beta binds to the SOCS3 promoter and represses SOCS

4 HNF-1beta binds to two evolutionarily conserved sites lo

5 HNF-1beta is a tissue-specific transcription factor that

6 HNF-1beta mutant cells also expressed lower levels of ch

7 HNF-1beta mutant kidneys showed increased expression of

8 HNF-4alpha gene silencing inhibited cell proliferation i

9 HNF-4alpha has a key role in regulating the multiple tra

10 HNF-4alpha is the most abundant DNA-binding protein in t

11 HNF-4alpha protein mutations are linked to maturity-onse

12 HNF-4alpha regulates a large number of liver-specific ge

13 HNF-4gamma, the other HNF-4 form highly expressed in int

14 HNF-6 and Notch signaling interact in vivo to control ex

15 HNF-6 expression was observed only in crypt epithelia ex

16 mammals, the OC family is comprised of OC-1/HNF-6, OC-2, and OC-3.

17 atory lesions compared with four of 21 (19%) HNF-1alpha-mutated, seven of 14 (50%) unclassified, and

18 A encoding hepatocyte nuclear factor 1alpha (HNF-1A) are associated with maturity-onset diabetes of t

19 naling via hepatocyte nuclear factor 1alpha (HNF-1alpha) compared with controls, which reduced expres

20 tations in hepatocyte nuclear factor 1alpha (HNF-1alpha).

21 s encoding hepatocyte nuclear factor-1alpha (HNF-1alpha) or HNF-4.

22 pends on interactions between the HNF-1alpha/HNF-4 signaling cascade and the serpin LCR.

23 ial role of hepatocyte nuclear factor-1beta (HNF-1beta) in regulating PPARGC1A expression in AKI.

24 Hepatocyte nuclear factor-1beta (HNF-1beta) is a homeodomain-containing transcription fac

25 Hepatocyte nuclear factor-1beta (HNF-1beta) is a Pit-1, Oct-1/2, Unc-86 (POU) homeodomain

26 Hepatocyte nuclear factor-1beta (HNF-1beta) is a transcription factor that regulates gene

27 tion factor hepatocyte nuclear factor-1beta (HNF-1beta) is essential for normal kidney development an

28 tion factor hepatocyte nuclear factor-1beta (HNF-1beta) regulates tissue-specific gene expression in

29 tion factor hepatocyte nuclear factor-1beta (HNF-1beta), mutations of which produce kidney cysts.

30 al similarity between HNF-1alpha and -1beta, HNF-1beta mutation carriers have hyperinsulinemia, where

31 , including hepatocyte nuclear factor 3beta (HNF-3beta), HNF-6alpha, CCAAT/enhancer binding protein a

32 hepatocyte nuclear factor 3beta (HNF-3beta), HNF-6alpha, CCAAT/enhancer binding protein alpha (C/EBPa

33 the binding of hepatocyte nuclear factor 4 (HNF-4), HNF-3, and fetoprotein factor to the precore/cor

34 ey hepatic factor, hepatic nuclear factor-4 (HNF-4), is crucial for the expression of many of these g

35 ding of hepatocyte nuclear factor 4 (HNF-4), HNF-3, and fetoprotein factor to the precore/core promot

36 receptors, hepatocyte nuclear factor 4alpha (HNF-4alpha) and alpha(1)-fetoprotein transcription facto

37 Hepatocyte nuclear factor 4alpha (HNF-4alpha) is a liver-enriched transcription factor tha

38 The hepatocyte nuclear factor 4alpha (HNF-4alpha; also known as NR2A1) is a member of the nucl

39 ctivity of hepatocyte nuclear factor-4alpha (HNF-4alpha) and peroxisome proliferators activated recep

40 X (MLX), and hepatic nuclear factor-4alpha (HNF-4alpha) are key transcription factors involved in th

41 e encoding hepatocyte nuclear factor-4alpha (HNF-4alpha) result in maturity-onset diabetes of the you

42 Hepatocyte nuclear factor-4alpha (HNF-4alpha), a liver-enriched transcription factor, is e

43 ncrease in hepatocyte nuclear factor-4alpha (HNF-4alpha), a liver-enriched, zinc-finger transcription

44 Hepatic nuclear factor-4alpha (HNF-4alpha), a transcription factor involved in the regu

45 r receptor hepatocyte nuclear factor-4alpha (HNF-4alpha), the gene that is mutated in Maturity-Onset

46 sly that hepatocyte nuclear receptor-4alpha (HNF-4alpha) controls intestinal epithelium homeostasis a

47 h signaling and hepatocyte nuclear factor-6 (HNF-6) are two genetic factors known to affect lineage c

48 40% of the actively transcribed genes have a HNF-4alpha response element.

49 tor PC4 display relatively robust activator (HNF-4)-dependent activity, which, nonetheless, can be fu

50 horylates HNF-4alpha, which directly affects HNF-4alpha activity.

51 (ChREBP), hepatocyte nuclear factor-4 alpha (HNF-4alpha) and peroxisome proliferative-activated recep

52 marked by hepatocyte nuclear factor 4 alpha (HNF-4alpha) expression] and cholangiocytes (marked by CK

53 show that hepatocyte nuclear factor 4 alpha (HNF-4alpha) plays a key role in controlling hepatic CES2

54 represses hepatocyte nuclear factor 4 alpha (HNF-4alpha)-activated PPAR-gamma2 gene expression by dir

55 endent on hepatocyte nuclear factor 4 alpha (HNF-4alpha; NR2A1), which itself regulates multiple live

56 sults suggest that the mechanism that alters HNF-4alpha binding after cytokine stimulation involves m

57 An HNF-1beta deletion mutant lacking the C-terminal domain

58 dgehogs in intestinal epithelial cells in an HNF-3beta (Foxa2)-dependent fashion.

59 Expression of an HNF-1beta C-terminal deletion mutant in transgenic mice

60 gene expression profiling, we found that an HNF-1beta target gene in the kidney is kinesin family me

61 The deletion of HNF-3 and HNF-6 binding sites within the LCR reduced histone acety

62 The amount of HNF-4 and HNF-3 was decreased posttranscriptionally by 8-1 in HBV-

63 s showed an interaction between ER-alpha and HNF-4alpha; this interaction prevented HNF-4alpha bindin

64 tions in HNF-1beta develop kidney cysts, and HNF-1beta regulates the transcription of several cystic

65 Furthermore, C/EBPbeta and HNF-6 proteins bound to the 3'RE region (+4647/+4694 bp)

66 he proteins encoded by Srebf2 and Hmgcr, and HNF-1beta directly controlled the renal epithelial expre

67 ic interaction involving Notch signaling and HNF-6 in mice has been inferred through separate experim

68 allothionein (MT), and cyclin D1, as well as HNF-4alpha.

69 In experimental assays, HNF-1A protein encoding the p.E508K mutant demonstrated

70 y increasing DRA expression via the RAR-beta/HNF-1beta-dependent pathway.

71 nce of 28 A was calculated from FRET between HNF-4alpha-E and cis-parinaric acid.

72 To define the genetic interaction between HNF-6 and Notch signaling in an in vivo mouse model, we

73 Despite structural similarity between HNF-1alpha and -1beta, HNF-1beta mutation carriers have

74 alpha but induce c-Jun, which in turn blocks HNF 4 alpha recruitment of PGC-1 alpha to the CYP7A1 chr

75 and RBP-J results in down-regulation of both HNF-1beta and Sox9 (sex determining region Y-related HMG

76 his in vivo model, simultaneous loss of both HNF-6 and RBP-J results in down-regulation of both HNF-1

77 with HNF-1alpha and inducing DNA binding by HNF-1alpha.

78 response to hepatic injury, characterized by HNF-4alpha silencing, impaired hepatocyte differentiatio

79 s and transcriptional programs controlled by HNF-1beta are poorly understood.

80 eutic approach for human diseases induced by HNF-1beta mutations.

81 ances liver regeneration at least in part by HNF-4alpha through the up-regulation of cell proliferati

82 -coding genes that are directly regulated by HNF-1beta in murine kidney epithelial cells.

83 RNAs (miRNAs) that are directly regulated by HNF-1beta in renal epithelial cells.

84 gions and are transcriptionally regulated by HNF-4alpha.

85 This may be mediated through regulation by HNF-1beta of the key gluconeogenic enzymes glucose-6-pho

86 cipitation assays and PCR analysis confirmed HNF-1beta binding to the Ppargc1a promoter in mouse kidn

87 genes encoding acute phase proteins contain HNF-4alpha-binding sites in their promoter regions and a

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

89 Here, we used Pkhd1/Cre mice to delete HNF-1beta specifically in renal collecting ducts (CDs).

90 Inhibition of p38 kinase activity diminishes HNF-4alpha nuclear protein levels and its phosphorylatio

91 al uncoupling was significantly higher in DN-HNF-1alpha cells, such that rates of ATP synthesis were

92 termediates revealed a negative impact of DN-HNF-1alpha and Hnf-1alpha knock-out on mitochondrial sec

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

94 uous to the surrounding cytoplasmic EpCAM(+)/HNF-4alpha(-) ductular oval cells.

95 +)) SHPC clusters showed membranous EpCAM(+)/HNF-4alpha(+) (hepatocyte nuclear factor-4alpha) stainin

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

97 ization cofactor of the transcription factor HNF-1.

98 ng site which binds the transcription factor HNF-1alpha.

99 e for the lung-specific transcription factor HNF-3beta and an E-box element in the distal enhancer ad

100 scription factor, hepatocyte nuclear factor (HNF) 1, plays a central role in liver gene regulation du

101 ide polymorphisms in hepatic nuclear factor (HNF) 1-alpha, a transcription factor with a wide range o

102 In addition, a hepatocyte nuclear factor (HNF) 3gamma-containing complex from prenatal liver inter

103 ved binding site for hepatic nuclear factor (HNF) 4alpha (-272/-252) was identified, which was requir

104 s have identified hepatocyte nuclear factor (HNF) 4alpha and insulin-like growth factor-binding prote

105 n (STAT) 5b, and for hepatic nuclear factor (HNF) 4alpha, as mediators of the sex-dependent effects o

106 P2D6) promoter by hepatocyte nuclear factor (HNF) 4alpha.

107 h inactivation of hepatocyte nuclear factor (HNF) 6 (Foxa3-Cre/Dicer(loxP/-)/Hnf6-/- mice).

108 arget of the LETF hepatocyte nuclear factor (HNF) 6.

109 The hepatocyte nuclear factor (HNF) family regulates complex networks of metabolism and

110 scription factors hepatocyte nuclear factor (HNF)-1alpha and -1beta result in MODY (maturity-onset di

111 protein levels of hepatocyte nuclear factor (HNF)-1alpha and retinoid X receptor (RXR)-alpha to inves

112 transcription factor hepatic nuclear factor (HNF)-1alpha, resulting in deficiency in glucose-stimulat

113 inflammatory, 20 hepatocyte nuclear factor (HNF)-1alpha-mutated, one beta-catenin-activated, and 14

114 , which binds the hepatocyte nuclear factor (HNF)-3beta.

115 transactivators, hepatocyte nuclear factor (HNF)-4alpha and HNF6.

116 gene encoding the hepatocyte nuclear factor (HNF)-4alpha are known to cause maturity-onset diabetes o

117 receptor (PPAR), hepatocyte nuclear factor (HNF)-4alpha, and liver X receptor (LXR) and the transcri

118 Overexpression of hepatocyte nuclear factor (HNF)-4alpha, which binds to this region, overcame the re

119 y interacted with hepatocyte nuclear factor (HNF)4alpha, an important transactivator of the human CYP

120 head homeobox A2, hepatocyte nuclear factor (HNF)4alpha, and HNF1alpha.

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

122 jury, providing evidence of a novel role for HNF-4alpha in the control of the liver's acute phase res

123 Foxa1, 2 and 3 (formerly HNF-3alpha, -beta and -gamma) constitute a sub-family of

124 d helix transcription factor Foxa2 (formerly HNF-3beta) in the pancreatic primordium during midgestat

125 No FRET from HNF-4alpha-E (amino acids 132-370) tryptophan (FRET dono

126 NA and miR-200 was decreased in kidneys from HNF-1beta knock-out mice and renal epithelial cells expr

127 Furthermore, HNF-4alpha nuclear expression is enhanced by inhibition

128 A crystal structure of the multidomain human HNF-4alpha homodimer bound to its DNA response element a

129 In HNF-4gamma knockout mice, we detect an exaggerated insul

130 -1beta subjects but was suppressed by 89% in HNF-1alpha subjects (P = 0.004) and 80% in control subje

131 onse is through site-specific alterations in HNF-4alpha-binding abilities and transactivation potenti

132 revealed downregulated expression of FXR in HNF-1beta mutant kidneys.

133 atment resulted in a significant increase in HNF-1beta mRNA levels.

134 pathway by insulin results in an increase in HNF-4alpha protein and a concomitant induction of 7alpha

135 200 targets, Zeb2 and Pkd1, was increased in HNF-1beta knock-out kidneys and in cells expressing muta

136 The expression of SOCS3 is increased in HNF-1beta knockout mice and in renal epithelial cells ex

137 n-regulated and cAMP levels are increased in HNF-1beta mutant kidney cells and mice.

138 te was not suppressed by low-dose insulin in HNF-1beta subjects but was suppressed by 89% in HNF-1alp

139 Humans with mutations in HNF-1beta develop kidney cysts, and HNF-1beta regulates

140 Studies were performed in HNF-4alpha-enriched HepG2 cells treated with cytokines f

141 decreased the expression of Zeb2 and Pkd1 in HNF-1beta mutant cells.

142 ralesional steatosis was exclusively seen in HNF-1alpha-mutated lesions.

143 a limited number of phosphorylation sites in HNF-4alpha have been identified, and the roles of HNF-4a

144 12 serine/threonine phosphorylation sites in HNF-4alpha.

145 of suppression of tumorigenicity 5 (ST5) in HNF-4alpha mutants, which we identify as a novel regulat

146 analysis revealed that phenobarbital-induced HNF-4alpha expression is both time- and dose dependent.

147 1 cells overexpressing doxycycline-inducible HNF-1alpha dominant-negative (DN-) gene mutations, and i

148 Expression of CAR inhibited HNF-4 transactivation of CYP7A1, a key gene in bile acid

149 Our data suggest that CAR inhibits HNF-4 activity by competing with HNF-4 for binding to th

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

151 rofiles from isolated islets of mice lacking HNF-4alpha in pancreatic beta-cells reveals that HNF-4al

152 assays indicate that wild-type, full-length HNF-4alpha (amino acids 1-455) has high affinity (Kd=0.0

153 ance energy transfer (FRET) from full-length HNF-4alpha tryptophan (FRET donor) to bound cis-parinaro

154 ay not reflect the properties of full-length HNF-4alpha.

155 chromatin immunoprecipitation analysis, less HNF-3beta was recruited to the apo A-I promoter in DHA-t

156 Compared with wild-type littermates, HNF-1beta mutant mice exhibited polyuria and polydipsia.

157 anscription of an HBV replicon with a mutant HNF-4alpha binding site within enhancer I.

158 k-out kidneys and in cells expressing mutant HNF-1beta.

159 Expression of dominant negative mutant HNF-1beta or kidney-specific inactivation of HNF-1beta d

160 al cells expressing dominant-negative mutant HNF-1beta rescues the defect in HGF-induced tubulogenesi

161 al cells expressing dominant-negative mutant HNF-1beta.

162 al cells expressing dominant-negative mutant HNF-1beta.

163 m mitigated the inhibitory effects of mutant HNF-1beta on the proteins encoded by Srebf2 and Hmgcr, a

164 estigated a controlled helical nanofilament (HNF: B4) phase under topographic confinement with airflo

165 The hepatocyte NF (HNF) family of transcription factors regulates the compl

166 DHA or PA had a similar nuclear abundance of HNF-3beta.

167 This is likely to reflect reduced action of HNF-1beta in the liver and possibly the kidney.

168 tly suppressed the DNA-binding activities of HNF-4alpha and PPAR-alpha, and reduced HNF-4alpha and PP

169 n assays, we determined that the activity of HNF-4alpha, a major regulator of apolipoprotein gene exp

170 ndicates that polymorphism of two alleles of HNF-4A gene (rs2144908 and rs1884614) and insulin recept

171 The amount of HNF-4 and HNF-3 was decreased posttranscriptionally by 8

172 ive mass spectrometry (MS)-based analysis of HNF-4alpha serine and threonine phosphorylation in respo

173 nobarbital treatment, whereas association of HNF-4 and coactivators, GRIP-1, p300, and PGC-1alpha, wi

174 at these polymorphisms affect the binding of HNF-1alpha and glucocorticoid receptor to the promoter,

175 mobility shift assays showed less binding of HNF-3beta to the -180 to -140 sequence of the apo A-I pr

176 oma HepG2 cells, DHA inhibits the binding of HNF-3beta to the apo A-I promoter, resulting in the repr

177 f an interference of DHA with the binding of HNF-3beta to the apo A-I promoter.

178 , which interacts with and alters binding of HNF-4alpha to the HBV enhancer I.

179 and ligand-induced conformational change of HNF-4alpha.

180 g partially through dimerization cofactor of HNF-1a (Dcoh2) Dcoh2, which increases dimerization of HN

181 part, on the intracellular concentrations of HNF-4alpha.

182 To determine the contribution of HNF-4alpha to the maintenance of glucose homeostasis by

183 of HNF1B leading to a superimposed defect of HNF-1beta transcriptional activity.

184 The deletion of HNF-3 and HNF-6 binding sites within the LCR reduced his

185 Surprisingly, deletion of HNF-4alpha in beta cells resulted in hyperinsulinemia in

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

187 coh2) Dcoh2, which increases dimerization of HNF-1alpha.

188 ion G20R perturbs the dimerization domain of HNF-1alpha, an intertwined four-helix bundle.

189 We conclude that the C-terminal domain of HNF-1beta is required for the activation of the Pkhd1 pr

190 Hence, the C-terminal F-domain of HNF-4alpha regulated ligand affinity, ligand specificity

191 Expression of HNF-1alpha in proximal tubules may protect against cysto

192 In conclusion, induced nuclear expression of HNF-4alpha and CAR is an integral part of the phenobarbi

193 In addition, nuclear expression of HNF-4alpha protein is significantly elevated 3 hours aft

194 arget genes responsible for the functions of HNF-1beta, however, is incompletely defined.

195 as a previously unrecognized target gene of HNF-1beta in the kidney.

196 HNF-1beta or kidney-specific inactivation of HNF-1beta decreased the expression of genes that are ess

197 Inactivation of HNF-1beta in mouse kidney tubules leads to early-onset c

198 to mice with kidney-specific inactivation of HNF-1beta.

199 t cytokine treatment leads to an increase of HNF-4alpha phosphorylation in several phosphopeptides.

200 II inhibitor KN62 block nuclear induction of HNF-4alpha by phenobarbital.

201 Moreover, inhibition of HNF-1beta significantly reduced PPARGC1A expression and

202 IFN-gamma and TNF-alpha led to inhibition of HNF-1beta transcriptional activity.

203 coactivators, potentiated CAR inhibition of HNF-4 transactivation.

204 mma2 gene expression by direct inhibition of HNF-4alpha transcriptional activity.

205 Knockout of HNF-1beta in the mouse kidney results in cyst formation.

206 n vivo, we derived a conditional knockout of HNF-4alpha using the Cre-loxP system.

207 n secretion with either mutations or loss of HNF-1alpha.

208 In conclusion, the loss of HNF-4gamma improves glucose homeostasis through a modula

209 xamined the effects of BHPC-specific loss of HNF-6 alone and within the background of BHPC-specific l

210 Isolated loss of HNF-6 in this mouse model fails to demonstrate a phenoty

211 Mutations of HNF-1beta cause maturity-onset diabetes of the young, ty

212 Mutations of HNF-1beta inhibited Kif12 transcription in both cultured

213 Mutations of HNF-1beta lead to a syndrome of inherited renal cysts an

214 Mutations of HNF-1beta produce congenital cystic abnormalities of the

215 fy multiple mechanisms, whereby mutations of HNF-1beta produce defects in urinary concentration.

216 1 expression, which argues that mutations of HNF-1beta produce kidney cysts by down-regulating the AR

217 Mutations of HNF-1beta produce kidney cysts, and previous studies hav

218 The phosphorylation of HNF-4alpha mediated by protein kinase A (PKA) significan

219 expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-in

220 ses alcoholic steatosis, and reactivation of HNF-4alpha and PPAR-alpha by increasing zinc availabilit

221 Here we show that the C-terminal region of HNF-1beta contains an activation domain that is function

222 ted the mechanism of metabolic regulation of HNF-1alpha/FXR signaling.

223 These findings reveal a novel role of HNF-1beta in a transcriptional network that regulates in

224 These findings reveal a novel role of HNF-1beta in osmoregulation and identify multiple mechan

225 in HepG2 cells, we investigated the role of HNF-4alpha in regulating the transcription of three HNF-

226 alpha have been identified, and the roles of HNF-4alpha phosphorylation after injury are unexplored.

227 However, the complete spectrum of HNF-1beta-regulated genes and pathways is not known.

228 not LCFA, altered the secondary structure of HNF-4alpha only when the F-domain was present.

229 igand specificity and secondary structure of HNF-4alpha.

230 ugh the production of 2HG and suppression of HNF-4alpha, a master regulator of hepatocyte identity an

231 cells and a direct transcriptional target of HNF-4alpha in vivo.

232 e Kir6.2 gene is a transcriptional target of HNF-4alpha.

233 00a/429) as novel transcriptional targets of HNF-1beta.

234 Treatment of HNF-1beta mutant mIMCD3 cells with hypertonic NaCl inhib

235 latively complex microscopic arrangements of HNFs compared with the B4 phase generated from the simpl

236 mimics the repressive effect of cytokines on HNF-4alpha binding, and the inhibition of PKA activity b

237 We studied the effects of phenobarbital on HNF-4alpha expression in hepatocytes and provide evidenc

238 tocyte nuclear factor-1alpha (HNF-1alpha) or HNF-4.

239 Although overexpressed ChREBP or HNF-4alpha did not relieve n-3 PUFA suppression of L-PK

240 L-PK) but did not suppress hepatic ChREBP or HNF-4alpha nuclear abundance.

241 impact L-PK promoter occupancy by ChREBP or HNF-4alpha.

242 HNF-4gamma, the other HNF-4 form highly expressed in intestine, is much less s

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

244 In the pancreas HNF-4alpha is also a master regulator, controlling an es

245 onal link between the p38 signaling pathway, HNF-4alpha, and bile acid synthesis.

246 Cytokine treatment phosphorylates HNF-4alpha, which directly affects HNF-4alpha activity.

247 a and HNF-4alpha; this interaction prevented HNF-4alpha binding to enhancer I and activation of HBV t

248 n 1), C/EBP (CCAAT/enhancer binding protein)/HNF-3beta (hepatocyte nuclear factor 3) and AP-1(activat

249 The F-domain of rat HNF-4alpha1 has a crucial impact on the ligand binding a

250 es of HNF-4alpha and PPAR-alpha, and reduced HNF-4alpha and PPAR-alpha target proteins.

251 ted in HepG2 cells with dramatically reduced HNF-4alpha protein concentrations.

252 a different set of 11 variants that reduced HNF-1A transcriptional activity to <60% of normal (wild-

253 inhibitor can partially recover the reduced HNF-4alpha binding activity induced by cytokines.

254 protein kinase A (PKA) significantly reduces HNF-4alpha binding activity, which mimics the repressive

255 SIRT1 regulated HNF-1alpha/FXR signaling partially through dimerization

256 n total HNF1A transcript levels but residual HNF-1alpha protein activity in G319S homozygotes may sti

257 pitation and sequencing experiments revealed HNF-1beta binding to the Nr1h4 promoter in wild-type kid

258 CD-specific HNF-1beta mutant mice survived long term and developed s

259 stimulation involves modulation of specific HNF-4alpha phosphorylation dependent, in part, on a PKA

260 enes, we examined whether CAR could suppress HNF-4 transactivation.

261 Our results demonstrate that HNF-4alpha is a crucial mediator in the regulation of al

262 Our data provide genetic evidence that HNF-4alpha is required in the pancreatic beta cell for r

263 ion in hepatocytes and provide evidence that HNF-4alpha nuclear expression is regulated in response t

264 Together, these results indicate that HNF-4alpha is essential for the physiological expansion

265 Pathway analysis predicted that HNF-1beta regulates cholesterol metabolism.

266 Thus, we propose that HNF-1beta links extracellular inflammatory signals to mi

267 merase chain reaction analyses revealed that HNF-4alpha mRNA is modestly up-regulated by phenobarbita

268 4alpha in pancreatic beta-cells reveals that HNF-4alpha regulates selected genes in the beta-cell, ma

269 l model of beta-cell expansion, we show that HNF-4alpha is required for beta-cell replication and the

270 the kidney, and previous studies showed that HNF-1beta regulates the expression of the autosomal rece

271 cysts, and previous studies have shown that HNF-1beta regulates the transcription of cystic disease

272 Our ChIP assay shows that HNF-1alpha and glucocorticoid receptor have stronger aff

273 The HNF-4alpha gene (HNF4A) resides on chromosome 20q12-q13.

274 tylation depends on interactions between the HNF-1alpha/HNF-4 signaling cascade and the serpin LCR.

275 Mutations of the HNF-1beta binding sites abolished promoter activity.

276 which overlapped with downregulation of the HNF-1beta transcriptional network.

277 The overall domain representation of the HNF-4alpha homodimer is different from that of the PPAR-

278 Targeting the HNF-4alpha/CES2 pathway may be useful for treatment of N

279 Luciferase reporter assays showed that the HNF-1beta binding sites were located within a promoter t

280 When applied to the HNF localization data in liver and pancreatic islets, ou

281 pha in regulating the transcription of three HNF-4alpha sensitive genes, alpha1-antitrypsin (alpha1-A

282 ssion is mediated, at least in part, through HNF-4alpha.

283 Thus, HNF-1beta regulates tubulogenesis by controlling the lev

284 (v) cis-Parinaric acid bound to HNF-4alpha with intact F-domain was readily displaceable

285 ctivation of the Pkhd1 promoter by wild-type HNF-1beta is stimulated by sodium butyrate or coactivato

286 e C-terminal domain interacts with wild-type HNF-1beta, binds DNA, and functions as a dominant-negati

287 However, when HNF-6 loss is combined with RBP-J loss, a phenotype cons

288 tion carriers have hyperinsulinemia, whereas HNF-1alpha mutation carriers have normal or reduced insu

289 These studies reveal a novel pathway whereby HNF-1beta directly contributes to the control of miRNAs

290 We examined whether HNF-1beta mutation carriers are insulin resistant.

291 The mechanism by which HNF-4alpha mediates this injury response is through site

292 While HNF-4alpha function is regulated by phosphorylation, onl

293 shift assays revealed that CAR competes with HNF-4 for binding to the DR1 motif in the CYP7A1 promote

294 GC-1alpha, indicating that CAR competes with HNF-4 for these coactivators.

295 AR inhibits HNF-4 activity by competing with HNF-4 for binding to the DR1 motif and to the common coa

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

297 tylate Dcoh2, promoting its interaction with HNF-1alpha and inducing DNA binding by HNF-1alpha.

298 f [6,6-(2)H(2)]glucose, in six subjects with HNF-1alpha mutations, six subjects with HNF-1beta mutati

299 Subjects with HNF-1beta mutations have reduced insulin sensitivity of

300 with HNF-1alpha mutations, six subjects with HNF-1beta mutations, and six control subjects, matched f