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 and beta-catenin/LEF compete for binding to th

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

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

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

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

8 HNF-1beta mutant kidneys showed increased expression of

9 HNF-4alpha gene silencing inhibited cell proliferation i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 tissue-specific transcription factor tha

27 Hepatocyte nuclear factor-1beta (HNF-1beta) is a tissue-specific transcription factor tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 terol-lowering compound which functions as a HNF-1alpha antagonist.

50 40% of the actively transcribed genes have a HNF-4alpha response element.

51 one enzyme-inorganic hybrid nanoflowers (ACC-HNFs) to fabricate high-performance artificial enzyme ca

52 Meticulous design of ACC-HNFs provided a versatile approach for constructing arti

53 Using paraoxon as a model analyte, the ACC-HNFs-based lab-on-paper platform could reach a limit of

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

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

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

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

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

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

60 erized by hepatocyte nuclear factor 4-alpha (HNF-4alpha) and albumin (ALB) expression and also analyz

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

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

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

64 inding factor (LEF) site overlapping with an HNF-1beta half-site.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 mode of active transcriptional repression by HNF-1beta.

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

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

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

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

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

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

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

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

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

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

100 ization cofactor of the transcription factor HNF-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Analysis of hepatocyte nuclear factors (HNFs) showed that transcription of HNF4alpha, which is k

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

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

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

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

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

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

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

131 -1beta subjects but was suppressed by 89% in HNF-1alpha subjects (P = 0.004) and 80% in control subje

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

133 e sites that are occupied by beta-catenin in HNF-1beta mutant cells colocalize with HNF-1beta-occupie

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

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

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

137 200 targets, Zeb2 and Pkd1, was increased in HNF-1beta knock-out kidneys and in cells expressing muta

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

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

140 on of Wnt target genes are also increased in HNF-1beta mutant mouse kidneys.

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

142 f the beta-catenin-binding domain of LEF1 in HNF-1beta-deficient cells abolishes the increase in Lef1

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

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

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

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

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

148 12 serine/threonine phosphorylation sites in HNF-4alpha.

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

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

151 1 cells overexpressing doxycycline-inducible HNF-1alpha dominant-negative (DN-) gene mutations, and i

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

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

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

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

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

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

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

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

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

161 Expression of dominant-negative mutant HNF-1beta in mIMCD3 cells produces hyperresponsiveness t

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

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

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

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

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

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

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

169 Ablation of HNF-1beta decreases H3K27 trimethylation repressive mark

170 Here, we show that ablation of HNF-1beta in mIMCD3 renal epithelial cells produces hype

171 Here, we show that ablation of HNF-1beta in mIMCD3 renal epithelial cells results in ac

172 ype and mutant cells showed that ablation of HNF-1beta increases by 6-fold the number of sites on chr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 Mutations of HNF-1beta produce congenital kidney abnormalities and in

217 Mutations of HNF-1beta produce cystic kidney disease, a phenotype ass

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

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

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

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

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

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

224 mono-methylation at the promoter regions of HNF-1alpha gene.

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

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

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

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

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

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

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

232 , is also a direct transcriptional target of HNF-1beta through binding to negative regulatory element

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

234 00a/429) as novel transcriptional targets of HNF-1beta.

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

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

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

238 knock-down abolished the effect of LASER on HNF-1alpha and PCSK9 expressions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 These findings demonstrate that HNF-1beta regulates canonical Wnt target genes through l

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

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

265 We found that HNF-1alpha and PCSK9 were reduced after LASER knock-down

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

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

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

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

270 4alpha in pancreatic beta-cells reveals that HNF-4alpha regulates selected genes in the beta-cell, ma

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

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

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

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

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

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

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

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

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

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

281 ete for binding to this element, and thereby HNF-1beta inhibits beta-catenin-dependent transcription.

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

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

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

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

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

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

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

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

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

291 in in HNF-1beta mutant cells colocalize with HNF-1beta-occupied sites in wild-type cells, indicating

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

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

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

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

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

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

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

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

300 WT HNF-1beta binds to two evolutionarily conserved sites lo

301 Mechanistically, WT HNF-1beta recruits the polycomb-repressive complex 2 tha