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1 ding a chloroplast dimerization co-factor of hepatocyte nuclear factor 1 (DCoH)/pterin-4alpha-carbino
2 GFBP-1 promoter activation was via an intact hepatocyte nuclear factor 1 (HNF-1) site and was depende
3 cells, we have identified a highly conserved hepatocyte nuclear factor 1 (HNF1) binding site residing
4 experimental process was defined by studying hepatocyte nuclear factor 1 (HNF1), which binds DNA as a
5 ing and for the transcription factor variant hepatocyte nuclear factor 1 (vhnf1) in specification of
6 th factor (Fgf) signals from r4; and variant hepatocyte nuclear factor 1 (vhnf1, also known as tcf2),
7 olamine dehydratase/dimerization cofactor of hepatocyte nuclear factor 1 alpha), a gene that was rece
8 odenal homeobox-1, BETA2/NeuroD, Nkx6.1, and hepatocyte nuclear factor 1 alpha), beta-cell metabolic
9 ntly down-regulated pathways associated with hepatocyte nuclear factor 1 homeobox A (Hnf1a) and hepat
13 cinomas, which expressed Napsin A and HNF1B (hepatocyte nuclear factor 1 homeobox B), markers of clea
15 lpha1-antitrypsin messenger RNA, albumin and hepatocyte nuclear factor 1 protein were detected in the
16 es for known trans-acting factors, including hepatocyte nuclear factor 1, Forkhead box A1 and CCCTC-b
18 ent genome-wide association study identified hepatocyte nuclear factor 1-alpha (HNF1A) as a key regul
19 48; 95% CI, 2.83-10.61; P = 4.4 x 10(-7)) in hepatocyte nuclear factor 1-alpha (HNF1A), the gene resp
20 the binding site of the transcription factor hepatocyte nuclear factor-1 (HNF-1) and specifically sup
21 , in LLC-PK cells, but not in HepG2 cells, a hepatocyte nuclear factor-1 (HNF-1) binding site was cri
23 arkedly decreases mRNA and protein levels of hepatocyte nuclear factor-1 (HNF-1), a transcription fac
25 zygous mutations in the transcription factor hepatocyte nuclear factor-1 alpha (HNF1A or TCF1 gene) r
26 mon polymorphisms of the HNF1A gene encoding hepatocyte nuclear factor-1 alpha and plasma C-reactive
27 tissue-specific transcription factor HNF-1 (hepatocyte nuclear factor-1) through binding the coactiv
29 subtypes based on inactivating mutations in hepatocyte nuclear factor 1A, activating mutations in be
30 subtypes based on inactivating mutations in hepatocyte nuclear factor 1A, activating mutations in be
34 nal farnesoid X receptor (FXR) signaling via hepatocyte nuclear factor 1alpha (HNF-1alpha) compared w
35 nts with diabetes caused by mutations in the hepatocyte nuclear factor 1alpha (HNF-1alpha) gene have
39 acious first-line treatment in patients with hepatocyte nuclear factor 1alpha (HNF1A) diabetes, but S
40 with glucokinase (GCK)-diabetes (MODY2) and hepatocyte nuclear factor 1alpha (HNF1A)-diabetes (MODY3
41 rotumoral interaction of Akt2 signaling with hepatocyte nuclear factor 1alpha (HNF1alpha) and PPARgam
42 ur previous in vitro studies have identified hepatocyte nuclear factor 1alpha (HNF1alpha) as an oblig
43 llular carcinoma development, directly binds hepatocyte nuclear factor 1alpha (HNF1alpha) mRNA, a neg
46 f hepatocyte-enriched transcription factors (hepatocyte nuclear factor 1alpha [HNF1alpha], -1beta, -3
47 adenomas combined with genetic analysis for hepatocyte nuclear factor 1alpha and beta-catenin mutati
49 ritical regulator of pregnane X receptor and hepatocyte nuclear factor 1alpha, and inactivation of th
50 rs, CCAAT/enhancer-binding protein alpha and Hepatocyte nuclear factor 1alpha, which are known to be
55 the cells with expression cassettes encoding hepatocyte nuclear factor-1alpha (HNF-1alpha) or HNF-4.
60 total HNF1A transcript levels, but residual hepatocyte nuclear factor-1alpha protein activity in G31
65 Here, we evaluated the potential role of hepatocyte nuclear factor-1beta (HNF-1beta) in regulatin
74 E4C is regulated by the transcription factor hepatocyte nuclear factor-1beta (HNF-1beta), mutations o
78 main that includes binding sites for NKX2.1, hepatocyte nuclear factor 3 (HNF-3), or cAMP response el
83 64A variant has a stronger homology with the hepatocyte nuclear factor 3 (HNF3)-binding site than +11
85 ng Sp1, Sp3, thyroid transcription factor 1, hepatocyte nuclear factor 3 and activating transcription
87 ated that PHx could induce the expression of hepatocyte nuclear factor 3 gamma (HNF3gamma) when viral
89 (CCAAT/enhancer binding protein)/HNF-3beta (hepatocyte nuclear factor 3) and AP-1(activator protein
90 overexpression of the transcription factors hepatocyte nuclear factor 3, octamer-binding protein 1,
91 a (FKHR), a recently described member of the hepatocyte nuclear factor 3/forkhead homeotic gene famil
93 e method to identify a previously unreported hepatocyte nuclear factor-3 site created in intron 8 of
94 istone H2A co-occupies, along with the FoxA (hepatocyte nuclear factor-3) transcription factor, DNA f
95 oic acid receptor, retinoic acid X receptor, hepatocyte nuclear factor-3, glucocorticoid receptor, nu
98 er-specific transcription factors, including hepatocyte nuclear factor 3beta (HNF-3beta), HNF-6alpha,
101 B virus (HBV) transgenic mice expressing rat hepatocyte nuclear factor 3beta (HNF3beta) were generate
102 of forkhead box A2 (FoxA2, previously called hepatocyte nuclear factor 3beta [HNF-3beta]), which caus
103 tion factor Foxa2 (Forkhead box a2, formerly Hepatocyte nuclear factor 3beta) in pancreatic beta cell
104 in which increased hepatic expression of the hepatocyte nuclear factor-3beta (HNF-3beta) protein was
105 tiated into epithelioid cells that expressed hepatocyte nuclear factor-3beta (HNF-3beta), GATA4, cyto
107 ker histone H5 and the DNA-binding domain of hepatocyte nuclear factor 3gamma (HNF-3gamma), making it
108 In this study, we cloned the cowpea bruchid hepatocyte nuclear factor 4 (CmHNF-4) and demonstrated i
110 l HBV promoters by decreasing the binding of hepatocyte nuclear factor 4 (HNF-4), HNF-3, and fetoprot
111 enes repressed by beta-catenin bind Tcf-4 on hepatocyte nuclear factor 4 (Hnf-4)-responsive elements.
114 expression of the nuclear hormone receptors hepatocyte nuclear factor 4 (HNF4) and the retinoid X re
117 reatly altering the efficiency of binding of hepatocyte nuclear factor 4 (HNF4) to this recognition s
120 enhances CYP2D6 promoter transactivation by hepatocyte nuclear factor 4 (HNF4alpha), a known transcr
121 ut model of the tumor-suppressive isoform of hepatocyte nuclear factor 4 alpha ("P1-HNF4alpha") in th
122 major isoforms of the transcription factor, hepatocyte nuclear factor 4 alpha (HNF-4 alpha), in live
123 lls give rise to both hepatocytes [marked by hepatocyte nuclear factor 4 alpha (HNF-4alpha) expressio
126 rol of some genes is critically dependent on hepatocyte nuclear factor 4 alpha (HNF-4alpha; NR2A1), w
128 , extracellular signal-related kinase (ERK), hepatocyte nuclear factor 4 alpha (HNF4A) and tumor necr
129 sion is enhanced by the transcription factor hepatocyte nuclear factor 4 alpha (HNF4A) through increa
131 ndependent microarray studies identified the hepatocyte nuclear factor 4 alpha (HNF4A), a transcripti
133 enriched OATP2B1 variant promoter identified hepatocyte nuclear factor 4 alpha (HNF4alpha) as a novel
134 ts the up-regulation and activation of human hepatocyte nuclear factor 4 alpha (HNF4alpha) in a p53-d
137 owed that over 83% of cells were albumin and hepatocyte nuclear factor 4 alpha (HNF4alpha) positive,
138 s constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce
141 ess maintained functional gene regulation by hepatocyte nuclear factor 4 alpha (HNF4alpha), whereas f
144 s, including six previously unknown loci (in hepatocyte nuclear factor 4 alpha [HNF4A], fucosyltransf
145 CPOBOP treatment caused transient decline in hepatocyte nuclear factor 4 alpha expression concomitant
146 Fs, CCAAT/enhancer-binding protein alpha and hepatocyte nuclear factor 4 alpha, in the livers of five
147 rate-responsive element-binding protein, and hepatocyte nuclear factor 4 alpha, were also found to be
149 we show that the nuclear hormone receptors, hepatocyte nuclear factor 4 and retinoid X receptor alph
151 d potential 20q candidates, including HNF4A (hepatocyte nuclear factor 4, alpha), TOMM34 (translocase
152 and mature hepatocytes were characterized by hepatocyte nuclear factor 4-alpha (HNF-4alpha) and album
154 otassium channel subunit Kir6.2 (KCNJ11) and hepatocyte nuclear factor 4-alpha (HNF4A) SNPs (0.01 < P
155 (n = 188), glucokinase (GCK)-MODY (n = 118), hepatocyte nuclear factor 4-alpha (HNF4A)-MODY (n = 40),
158 physically and functionally interacted with hepatocyte nuclear factor-4 alpha (HNF-4 alpha), a nucle
159 e response element-binding protein (ChREBP), hepatocyte nuclear factor-4 alpha (HNF-4alpha) and perox
162 cyte nuclear factor 1 homeobox A (Hnf1a) and hepatocyte nuclear factor 4A (Hnf4a), known modifiers of
163 e network, which was down-regulated in mouse hepatocyte nuclear factor 4A knockout mice; were early-s
164 ass represented 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven gene network, which
168 ired for binding of the transcription factor hepatocyte nuclear factor 4alpha (HNF-4alpha) to the pro
170 of upstream transcription factors, including hepatocyte nuclear factor 4alpha (Hnf4a) and Hnf1a, as w
172 ry regions bound by the transcription factor hepatocyte nuclear factor 4alpha (HNF4A) was reduced dur
175 er, PGC-1alpha is induced and interacts with hepatocyte nuclear factor 4alpha (HNF4alpha) and other t
176 on was found to be under the control of both hepatocyte nuclear factor 4alpha (HNF4alpha) and peroxis
178 nal link between the orphan nuclear receptor hepatocyte nuclear factor 4alpha (HNF4alpha) and transcr
179 tional knockout mice have shown that loss of hepatocyte nuclear factor 4alpha (HNF4alpha) blocks the
180 ure assays were employed to demonstrate that hepatocyte nuclear factor 4alpha (HNF4alpha) bound to th
184 o decreased by 45% in the setting of reduced hepatocyte nuclear factor 4alpha (HNF4alpha) expression.
187 enesis by targeting the gluconeogenic factor hepatocyte nuclear factor 4alpha (HNF4alpha) in both cel
200 zation of tumor suppressor proteins Rb, p53, hepatocyte nuclear factor 4alpha (HNF4alpha), and CCAAT/
201 ), LXRalpha, liver receptor homolog (LRH-1), hepatocyte nuclear factor 4alpha (HNF4alpha), and short
202 oters including the glucocorticoid receptor, hepatocyte nuclear factor 4alpha (HNF4alpha), and the pe
203 /arginine-rich splicing factor 3 (Srsf3) and hepatocyte nuclear factor 4alpha (Hnf4alpha), and was cr
204 ion of a known positive regulator of CYP2D6, hepatocyte nuclear factor 4alpha (HNF4alpha), did not ch
209 r data show that PGC-1alpha interaction with hepatocyte nuclear factor 4alpha (HNF4alpha, NR2A1) dire
210 ing protein-1c (SREBP-1c) strongly inhibited hepatocyte nuclear factor 4alpha and peroxisome prolifer
212 ntrol on the hepatocyte transcription factor hepatocyte nuclear factor 4alpha by modulating its activ
213 matrigel, suggesting that down-regulation of hepatocyte nuclear factor 4alpha expression is involved
216 R-specific agonist and adenovirus expressing hepatocyte nuclear factor 4alpha or constitutively activ
217 X-Gal staining showed Adamts7 expression in hepatocyte nuclear factor 4alpha(+) hepatocytes and desm
218 ICD) mice is accompanied by re-expression of hepatocyte nuclear factor 4alpha(HNF4alpha), possibly in
220 damage, increase in expression of HNF4alpha (hepatocyte nuclear factor 4alpha), a key driver associat
221 The tumor cells coexpressed hepatocyte (hepatocyte nuclear factor 4alpha), progenitor/biliary (k
222 were found in the perigenic regions: HNF4A (hepatocyte nuclear factor 4alpha), SLC12A5 (potassium-ch
223 the presence of the liver-specific markers, hepatocyte nuclear factor 4alpha, albumin, cytokeratin 1
224 way linking FXR to changes in hepatic p-JNK, hepatocyte nuclear factor 4alpha, and finally SR-BI.
225 indicated that viral replication mediated by hepatocyte nuclear factor 4alpha, retinoid X receptor al
226 acid receptor, the retinoid X receptor, the hepatocyte nuclear factor 4alpha, the chicken ovalbumin
227 l cell adhesion molecule-negative (EpCAM(-)) hepatocyte nuclear factor 4alpha-positive (HNF4alpha(+))
231 ich was accompanied by restoring activity of hepatocyte nuclear factor-4alpha (HNF-4alpha) and peroxi
234 eneration was associated with an increase in hepatocyte nuclear factor-4alpha (HNF-4alpha), a liver-e
235 s-regulatory element transcription factor as hepatocyte nuclear factor-4alpha (HNF-4alpha), and confi
236 is dependent on the orphan nuclear receptor hepatocyte nuclear factor-4alpha (HNF-4alpha), the gene
237 d the CAR-dependent inhibition was linked to hepatocyte nuclear factor-4alpha (HNF4alpha)-mediated tr
238 ere we show that the orphan nuclear receptor hepatocyte nuclear factor-4alpha (HNF4alpha; HNF4A) is c
241 ivated receptor gamma coactivator 1alpha and hepatocyte nuclear factor-4alpha were increased in IUGR
242 rs showed membranous EpCAM(+)/HNF-4alpha(+) (hepatocyte nuclear factor-4alpha) staining and were cont
243 or PGC-1alpha partners, including PPARalpha, hepatocyte nuclear factor-4alpha, and estrogen receptor
244 ryl hydrocarbon receptor, but not of CYP3A4, hepatocyte nuclear factor-4alpha, or pregnane X receptor
245 epatocyte transcriptional factors, including hepatocyte nuclear factor-4alpha, that is early down-reg
253 complexes between the DNA-binding domains of hepatocyte nuclear factor 6 (HNF6) and forkhead box a2 (
254 lexes between the DNA binding domains of the hepatocyte nuclear factor 6 (HNF6) and Forkhead Box a2 (
255 xplore the requirement for downregulation of hepatocyte nuclear factor 6 (HNF6) expression in the ass
258 regulated transcriptional activators (STAT5, hepatocyte nuclear factor 6 [HNF6], FOXA1, and FOXA2) an
259 ts was positively correlated (p < 0.05) with hepatocyte nuclear factor 6 and estrogen receptor-alpha
263 Our results indicate that binding sites for hepatocyte nuclear factors (especially HNF-1 and HNF-4)
264 e mouse Oatp4 putative response elements for hepatocyte nuclear factor (HNF) 1, CAAT/enhancer binding
265 homeodomain-containing transcription factor, hepatocyte nuclear factor (HNF) 1, plays a central role
266 n activity was obtained by cotransfection of hepatocyte nuclear factor (HNF) 3gamma or HNF4alpha.
268 Our recent DNA microarrays have identified hepatocyte nuclear factor (HNF) 4alpha and insulin-like
273 ice), combined (or not) with inactivation of hepatocyte nuclear factor (HNF) 6 (Foxa3-Cre/Dicer(loxP/
276 pancreatic transcription factors, including hepatocyte nuclear factor (HNF)-1 and HNF-3, form a tigh
277 estine-specific Cdx homeodomain proteins and hepatocyte nuclear factor (HNF)-1, which are conserved i
279 ygous mutations in the transcription factors hepatocyte nuclear factor (HNF)-1alpha and -1beta result
280 ansporters; and 4) nuclear protein levels of hepatocyte nuclear factor (HNF)-1alpha and retinoid X re
281 ucokinase (GCK) and the transcription factor hepatocyte nuclear factor (HNF)-1alpha are the most comm
283 ysiology of the beta-cell, with mutations in hepatocyte nuclear factor (HNF)-1alpha, HNF-4alpha, insu
284 were subclassified into 14 inflammatory, 20 hepatocyte nuclear factor (HNF)-1alpha-mutated, one beta
288 tations in the human HNF4A gene encoding the hepatocyte nuclear factor (HNF)-4alpha are known to caus
290 some proliferator-activated receptor (PPAR), hepatocyte nuclear factor (HNF)-4alpha, and liver X rece
293 x1 strongly and specifically interacted with hepatocyte nuclear factor (HNF)4alpha, an important tran
294 enes such as glucagon, forkhead homeobox A2, hepatocyte nuclear factor (HNF)4alpha, and HNF1alpha.
296 Foxa3 (HNF-3gamma) act in concert with other hepatocyte nuclear factors (HNF) to coordinately regulat
299 The hepatic promoter depends on a cluster of hepatocyte nuclear factor sites 123-155 bp upstream of t
300 including C/EBP, nuclear factor-kappaB, and hepatocyte nuclear factor were found in the region upstr