Relevant bibliographies by topics / Hepatocyte nuclear factor

Academic literature on the topic 'Hepatocyte nuclear factor'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Hepatocyte nuclear factor"

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Eeckhoute, J. "Hepatocyte Nuclear Factor 4 enhances the Hepatocyte Nuclear Factor 1 -mediated activation of transcription." Nucleic Acids Research 32, no. 8 (April 28, 2004): 2586–93. http://dx.doi.org/10.1093/nar/gkh581.

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Sund, Newman J., Siew-Lan Ang, Sara Dutton Sackett, Wei Shen, Nathalie Daigle, Mark A. Magnuson, and Klaus H. Kaestner. "Hepatocyte Nuclear Factor 3β (Foxa2) Is Dispensable for Maintaining the Differentiated State of the Adult Hepatocyte." Molecular and Cellular Biology 20, no. 14 (July 15, 2000): 5175–83. http://dx.doi.org/10.1128/mcb.20.14.5175-5183.2000.

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ABSTRACT Liver-specific gene expression is controlled by a heterogeneous group of hepatocyte-enriched transcription factors. One of these, the winged helix transcription factor hepatocyte nuclear factor 3β (HNF3β or Foxa2) is essential for multiple stages of embryonic development. Recently, HNF3β has been shown to be an important regulator of other hepatocyte-enriched transcription factors as well as the expression of liver-specific structural genes. We have addressed the role of HNF3β in maintenance of the hepatocyte phenotype by inactivation ofHNF3β in the liver. Remarkably, adult mice lackingHNF3β expression specifically in hepatocytes are viable, with histologically normal livers and normal liver function. Moreover, analysis of >8,000 mRNAs by array hybridization revealed that lack ofHNF3β affects the expression of only very few genes. Based on earlier work it appears that HNF3β plays a critical role in early liver development; however, our studies demonstrate that HNF3β is not required for maintenance of the adult hepatocyte or for normal liver function. This is the first example of such functional dichotomy for a tissue specification transcription factor.
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ULVILA, Johanna, Satu ARPIAINEN, Olavi PELKONEN, Kaoru AIDA, Tatsuya SUEYOSHI, Masahiko NEGISHI, and Jukka HAKKOLA. "Regulation of Cyp2a5 transcription in mouse primary hepatocytes: roles of hepatocyte nuclear factor 4 and nuclear factor I." Biochemical Journal 381, no. 3 (July 27, 2004): 887–94. http://dx.doi.org/10.1042/bj20040387.

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The cytochrome P4502a5 (Cyp2a5) gene is expressed principally in liver and olfactory mucosa. In the present study, the transcriptional mechanisms of hepatocyte-specific expression of Cyp2a5 were studied in mouse primary hepatocytes. The Cyp2a5 5′-flanking region −3033 to +10 was cloned in front of a luciferase reporter gene and transfected into hepatocytes. Deletion analysis revealed two major activating promoter regions localized at proximal 271 bp and at a more distal area from −3033 to −2014 bp. The proximal activation region was characterized further by DNase I footprinting, and a single clear footprint was detected in the studied area centred over a sequence similar to the NF-I (nuclear factor I)-binding site. The binding of NF-I was confirmed using an EMSA (electrophoretic mobility-shift assay). A putative HNF-4 (hepatocyte nuclear factor 4)-binding site was localized at the proximal promoter by computer analysis of the sequence, and HNF-4α was shown to interact with the site using an EMSA. The functional significance of HNF-4 and NF-I binding to the Cyp2a5 promoter was evaluated by site-directed mutagenesis of the binding motifs in reporter constructs. Both mutations strongly decreased transcriptional activation by the Cyp2a5 promoter in primary hepatocytes, and double mutation almost completely abolished transcriptional activity. Also, the functionality of the distal activation region was found to be dependent on the intact HNF-4 and NF-I sites at the proximal promoter. In conclusion, these results indicate that HNF-4 and NF-I play major roles in the constitutive regulation of hepatic expression of Cyp2a5.
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Wang, Zhongyan, and Peter A. Burke. "Hepatocyte nuclear factor-4α interacts with other hepatocyte nuclear factors in regulating transthyretin gene expression." FEBS Journal 277, no. 19 (August 23, 2010): 4066–75. http://dx.doi.org/10.1111/j.1742-4658.2010.07802.x.

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Gardner-Stephen, Dione A., and Peter I. Mackenzie. "Hepatocyte nuclear factor1 transcription factors are essential for the UDP-glucuronosyltransferase 1A9 promoter response to hepatocyte nuclear factor 4α." Pharmacogenetics and Genomics 17, no. 1 (January 2007): 25–36. http://dx.doi.org/10.1097/fpc.0b013e32801112b5.

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Khurana, Satish, Amit K. Jaiswal, and Asok Mukhopadhyay. "Hepatocyte Nuclear Factor-4α Induces Transdifferentiation of Hematopoietic Cells into Hepatocytes." Journal of Biological Chemistry 285, no. 7 (December 16, 2009): 4725–31. http://dx.doi.org/10.1074/jbc.m109.058198.

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Tian, J. M., and U. Schibler. "Tissue-specific expression of the gene encoding hepatocyte nuclear factor 1 may involve hepatocyte nuclear factor 4." Genes & Development 5, no. 12a (December 1, 1991): 2225–34. http://dx.doi.org/10.1101/gad.5.12a.2225.

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Aboudehen, Karam, Min Soo Kim, Matthew Mitsche, Kristina Garland, Norma Anderson, Lama Noureddine, Marco Pontoglio, et al. "Transcription Factor Hepatocyte Nuclear Factor–1βRegulates Renal Cholesterol Metabolism." Journal of the American Society of Nephrology 27, no. 8 (December 28, 2015): 2408–21. http://dx.doi.org/10.1681/asn.2015060607.

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Freedman, A. R., R. J. Sharma, G. J. Nabel, S. G. Emerson, and G. E. Griffin. "Cellular distribution of nuclear factor κB binding activity in rat liver." Biochemical Journal 287, no. 2 (October 15, 1992): 645–49. http://dx.doi.org/10.1042/bj2870645.

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The cellular localization of nuclear factor kappa B (NF-kappa B) binding activity in rat liver has been investigated using electrophoretic mobility shift assay on extracts of highly purified hepatocytes and Kupffer cells obtained from liver perfused in vivo with collagenase. Constitutive NF-kappa B binding activity was demonstrated in nuclear extracts of control Kupffer cells, and this was not apparently influenced by injection of lipopolysaccharide (LPS) into rats 24 h before perfusion. In contrast, little nuclear NF-kappa B binding activity was present in hepatocytes from control animals, although there was detectable inactive, inhibitor-bound, NF-kappa B in the cytoplasm. However, nuclear NF-kappa B binding activity was increased in hepatocytes from LPS-treated animals and after in vitro culture of control rat hepatocytes. Thus NF-kappa B binding activity has been demonstrated in highly purified hepatocytes and appears to be inducible both in vivo and in vitro. These findings support a role for NF-kappa B in hepatocyte gene regulation which may be important in the modulation of the hepatic acute phase response.
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Tang, Hong, and Alan McLachlan. "Avian and Mammalian Hepadnaviruses Have Distinct Transcription Factor Requirements for Viral Replication." Journal of Virology 76, no. 15 (August 1, 2002): 7468–72. http://dx.doi.org/10.1128/jvi.76.15.7468-7472.2002.

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ABSTRACT Hepadnavirus replication occurs in hepatocytes in vivo and in hepatoma cell lines in cell culture. Hepatitis B virus (HBV) replication can occur in nonhepatoma cells when pregenomic RNA synthesis from viral DNA is activated by the expression of the nuclear hormone receptors hepatocyte nuclear factor 4 (HNF4) and the retinoid X receptor α (RXRα) plus peroxisome proliferator-activated receptor α (PPARα) heterodimer. Nuclear hormone receptor-dependent HBV replication is inhibited by hepatocyte nuclear factor 3 (HNF3). In contrast, HNF3 and HNF4 support duck hepatitis B virus (DHBV) replication in nonhepatoma cells, whereas the RXRα-PPARα heterodimer inhibits HNF4-dependent DHBV replication. HNF3 and HNF4 synergistically activate DHBV pregenomic RNA synthesis and viral replication. The conditions that support HBV or DHBV replication in nonhepatoma cells are not able to support woodchuck hepatitis virus replication. These observations indicate that avian and mammalian hepadnaviruses have distinct transcription factor requirements for viral replication.
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Dissertations / Theses on the topic "Hepatocyte nuclear factor"

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Clissold, Rhian. "Identification of hepatocyte nuclear factor 1β-associated disease." Thesis, University of Exeter, 2017. http://hdl.handle.net/10871/31132.

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Heterozygous mutations and deletions of the gene that encodes the transcription factor hepatocyte nuclear factor 1β (HNF1B) are the commonest known monogenic cause of developmental kidney disease. However, diagnosis remains challenging due to phenotypic variability and frequent absence of a family history. There is also no consensus as to when HNF1B genetic testing should be performed. This thesis includes work looking at the identification of HNF1B-associated disease. An HNF1B score was developed in 2014 to help select appropriate patients for genetic testing. The aim in chapter 2 was to test the clinical utility of this score in a large number of referrals for HNF1B genetic testing to the UK diagnostic testing service for the HNF1B gene. An HNF1B score was assigned for 686 referrals using clinical information available at the time of testing; performance of the score was evaluated by receiver-operating characteristic curve analysis. Although the HNF1B score discriminated between patients with and without a mutation/deletion reasonably well, the negative predictive value of 85% reduces its clinical utility. HNF1B-associated disease is due to an approximate 1.3 Mb deletion of chromosome 17q12 in about 50% of individuals. This deletion includes HNF1B plus 14 additional genes and has been linked to an increased risk of neurodevelopmental disorders, such as autism. The aim in chapter 3 was to compare the neurodevelopmental phenotype of patients with either an HNF1B intragenic mutation or 17q12 deletion to determine whether haploinsufficiency of the HNF1B gene is responsible for this aspect of the phenotype. Brief behavioural screening showed high levels of psychopathology and impact in children with a deletion. 8/20 (40%) patients with a deletion had a clinical diagnosis of a neurodevelopmental disorder compared to 0/18 with a mutation, P=0.004. 17q12 deletions were also associated with more autistic traits. Two independent clinical geneticists were able to predict the presence of a deletion with a sensitivity of 83% and specificity of 79% when assessing facial dysmorphic features as a whole. These results demonstrate that the 17q12 deletion but not HNF1B intragenic mutations are associated with neurodevelopmental disorders; we conclude that the HNF1B gene is not involved in the neurodevelopmental phenotype of these patients. Extra-renal phenotypes frequently occur in HNF1B-associated disease, including diabetes mellitus and pancreatic hypoplasia. Faecal elastase-1 levels have only been reported in a small number of individuals, the majority of which have diabetes. In chapter 4 we measured faecal elastase-1 in patients with an HNF1B mutation or deletion regardless of diabetes status and assessed the degree of symptoms associated with pancreatic exocrine deficiency. We found that faecal elastase-1 deficiency is a common feature of HNF1B-associated renal disease even when diabetes is not present and pancreatic exocrine deficiency may be more symptomatic than previously suggested. Faecal elastase-1 should be measured in all patients with a known HNF1B molecular abnormality complaining of chronic abdominal pain, loose stools or unintentional weight loss. Hypomagnesaemia is a common feature of HNF1B-associated disease and is due to renal magnesium wasting. The aim in chapter 5 was to measure both serum and urine magnesium and calcium levels in individuals with an HNF1B molecular defect and compare to a cohort of patients followed up in a general nephrology clinic in order to assess their potential as biomarkers for HNF1B-associated disease. The results of this pilot study show that using a cut-off for serum magnesium of ≤0.75 mmol/L was 100% sensitive and 87.5% specific for the presence of an HNF1B mutation/deletion. All individuals in the HNF1B cohort had hypermagnesuria with fractional excretion of magnesium >4%; a cut-off of ≥4.1% was 100% sensitive and 71% specific. This suggests serum magnesium levels and fractional excretion of magnesium are highly sensitive biomarkers for HNF1B-associated renal disease; if these results are confirmed in a larger study of patients with congenital anomalies of the kidneys or urinary tract they could be implemented as cheap screening tests for HNF1B genetic testing in routine clinical care.
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Bingham, Coralie. "The renal manifestations of hepatocyte nuclear factor mutations." Thesis, University of Exeter, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269720.

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Hannoun, Zara. "Role of SUMO modification in hepatocyte differentiation." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5917.

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Primary human hepatocytes are a scarce resource with variable function, which diminishes with time in culture. As a consequence their use in tissue modelling and therapy is restricted. Human embryonic stem cells (hESCs) could provide a stable source of human tissue due to their properties of self-renewal and their ability to give rise to all three germ layers. hESCs have the potential to provide an unlimited supply of hepatic endoderm (HE) which could offer efficient tools for drug discovery, disease modelling and therapeutic applications. In order to create a suitable environment to enhance HE formation, hESC culture needed to be standardised. As such, a media trail was carried out to define serum free media capable of maintaining hESC in a pluripotent undifferentiated state. We also ensured hESC cultured in the various media could be directly differentiated to HE in a reproducible and efficient manner. The project then focused on the effect of post-translational modifications (PTMs), specifically SUMOylation, in hepatocyte differentiation and its subsequent manipulation to enhance HE viability. SUMOylation is a PTM known to modify a large number of proteins that play a role in various cellular processes including: cell cycle regulation, gene transcription, differentiation and cellular localisation. We hypothesised that SUMO modification may not only regulate hESC self renewal, but also maybe required for efficient hESC differentiation. We therefore interrogated the role of SUMOylation in hESC differentiation to hepatic endoderm (HE). hESC were differentiated and the cellular lysates were analysed by Western blotting for key proteins which modulate the conjugation and de conjugation of SUMO. We demonstrate that peak levels of SUMOylation were detectable in hESC populations and during cellular differentiation to definitive endoderm (DE), day 5. Following commitment to DE we observed a decrease in the level of SUMO modified proteins during cellular specialisation to a hepatic fate, corresponding with an increase in SENP 1, a SUMO deconjugation enzyme. We also detected reduced levels of hepatocyte nuclear factor 4 α (HNF4α), a critical regulator of hepatic status and metabolic function, as SUMOylation decreased. As a result, we investigated if HNF4α was SUMOylated and if this process was involved in modulating HNF4α’s critical role in HE. HNF4α is an important transcription factor involved in liver organogenesis during development and is a key regulator for efficient adult liver metabolic functions. We observed a decreasing pattern of HNF4α expression at day 17 of our differentiation protocol in conjunction with a decrease in SUMO modified proteins. In order to further investigate and validate a role of SUMOylation on HNF4α stability Immunoprecipitation (IP) was employed. HNF4α protein was pulled down and probed for SUMO 2. Results show an increase in the levels of SUMO2 modification as the levels of HNF4α decrease. Through deletion and mutation analysis we demonstrated that SUMO modification of HNF4α was restricted to the C-terminus on lysine 365. Protein degradation via the proteasome was responsible for the decrease in HNF4α, demonstrated by the use of a proteasome 26S inhibitor MG132. Additionally, a group at the University of Dundee has shown that polySUMOylation of promyelocytic leukaemia protein (PML) leads to its subsequent ubiquitination via RNF4, an ubiquitin E3 ligase, driving its degradation. Using an in vitro ubiquitination assay, we show that polySUMOylated HNF4α is preferentially ubiquitinated in the presence of RNF4. Overall polySUMOylation of HNF4α may reduce its stability by driving its degradation, hence regulating protein activity. In conclusion, polySUMOylation of HNF4α is associated with its stability. HNF4α is subsequently important for HE differentiation both driving the formation of the hepatocytes and in maintaining a mature phenotype, in agreement with a number of different laboratories. Creating the ideal environment for sustaining mature functional hepatocytes, primary and those derived from hESCs and iPSCs, is essential for further use in applications such as drug screening, disease modelling and extracorporeal devices.
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Chéret, Claire. "Spécificité et redondance des facteurs de transcription HNF1α (Hepatocyte Nuclear Factor-1α) et HNF1β/vHNF1 (Hepatocyte Nuclear Factor-1β/variant HNF1) chez la souris." Paris 6, 2002. http://www.theses.fr/2002PA066076.

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Gresh, Lionel. "Rôles du facteur de transcription hepatocyte nuclear factor 1beta au cours de l'organogenèse." Paris 6, 2004. http://www.theses.fr/2004PA066143.

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Chellappa, Karthikeyani. "Functional analysis of Tyrosine residues in human hepatocyte nuclear factor 4alpha." Diss., UC access only, 2009. http://proquest.umi.com/pqdweb?index=72&did=1790348311&SrchMode=1&sid=1&Fmt=7&retrieveGroup=0&VType=PQD&VInst=PROD&RQT=309&VName=PQD&TS=1270229827&clientId=48051.

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Thesis (Ph. D.)--University of California, Riverside, 2009.
Includes abstract. Includes bibliographical references (leaves 293-348). Issued in print and online. Available via ProQuest Digital Dissertations.
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Marable, Sierra S. "The Role of Hepatocyte Nuclear Factor 4a in Renal Proximal Tubule Development." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595849621045508.

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Papachristodoulou, Maria. "A study of the ligand-binding properties of hepatocyte nuclear factor 4α (HNF4α)." Thesis, University of Surrey, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429895.

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Xu, Jianyu. "Mutations in the hepatocyte nuclear factor 1 and glucokinase genes in Southern Chinese patients with early-onset type 2 diabetes." Click to view the E-thesis via HKUTO, 2002. http://sunzi.lib.hku.hk/hkuto/record/B42576854.

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Karatza, Panagiota. "Characterization and functional analysis of the hepatocyte nuclear factor 1 alpha 5'-flanking region." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423198.

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Books on the topic "Hepatocyte nuclear factor"

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Bingham, Coralie. Hepatocyte nuclear factor-1B. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0315_update_001.

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Hepatocyte nuclear factor-1B (HNF1B, also known as TCF2) is a transcription factor that is involved in renal development, and in the transcription of several genes implicated in other genetic renal diseases. Mutations in HNF1B cause maturity onset diabetes of the young, renal cysts and diabetes syndrome, and some cases of familial juvenile hyperuricaemic nephropathy. They also account for a large proportion of developmental renal disorders included abnormalities detected antenatally. The various abnormalities associated with the gene may occur in isolation or together in the same patient.
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Differential Induction of Nuclear Factor-κB and Activator Protein-1 Activity after CD40 Ligation Is Associated with Primary Human Hepatocyte Apoptosis or Intrahepatic Endothelial Cell Proliferation. Molecular Biology of the Cell, 2003.

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Book chapters on the topic "Hepatocyte nuclear factor"

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Stoffel, Markus. "The Role of the Hepatocyte Nuclear Factor Network in Glucose Homeostasis." In Molecular Basis of Pancreas Development and Function, 255–74. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_15.

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Shiota, Goshi, and Yoko Yoshida. "“Tet-On” System Toward Hepatic Differentiation of Human Mesenchymal Stem Cells by Hepatocyte Nuclear Factor." In Methods in Molecular Biology, 125–32. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-468-1_11.

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Stoffel, M. "Role of the Hepatocyte Nuclear Factor Network in Maturity-Onset Diabetes of the Young (MODY)." In Frontiers in Diabetes, 251–64. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000060928.

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Pinaire, Jane, Wan-Yin Chou, Mark Stewart, Katrina Dipple, and David Crabb. "Activity of the Human Aldehyde Dehydrogenase 2 Promoter Is Influenced by the Balance between Activation by Hepatocyte Nuclear Factor 4 and Repression by Perosixome Proliferator Activated Receptor δ, Chicken Ovalbumin Upstream Promoter-Transcription Factor, and Apolipoprotein Regulatory Protein-1." In Advances in Experimental Medicine and Biology, 115–21. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4735-8_14.

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Sladek, Frances M., and Shawn D. Seidel. "Hepatocyte Nuclear Factor 4α." In Nuclear Receptors and Genetic Disease, 309–61. Elsevier, 2001. http://dx.doi.org/10.1016/b978-012146160-7/50010-x.

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Bingham, Coralie. "Hepatocyte nuclear factor-1B." In Oxford Textbook of Clinical Nephrology, 2671–73. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0315.

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"HNF (hepatocyte nuclear factor)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 888. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_7711.

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"Hepatocyte nuclear factor-2." In Springer Reference Medizin, 1103. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_311774.

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Owen, K., G. Thanabalasingham, and AJ Juszczak. "MODY due to hepatocyte nuclear factor 4-alpha mutations (revision number 10)." In Diapedia. Diapedia.org, 2012. http://dx.doi.org/10.14496/dia.41040851228.10.

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Owen, K., G. Thanabalasingham, and AJ Juszczak. "MODY due to hepatocyte nuclear factor 4-alpha mutations (revision number 11)." In Diapedia. Diapedia.org, 2014. http://dx.doi.org/10.14496/dia.41040851228.11.

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Conference papers on the topic "Hepatocyte nuclear factor"

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Ning, Bei-Fang, Xin Zhang, and Wei-Fen Xie. "Abstract 2463: Suppression of hepatocyte nuclear factor 4α by nuclear factor κB in hepatoma cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2463.

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Yamashita, Taro, Hikari Okada, Masao Honda, and Shuichi Kaneko. "Abstract 1904: Polyprenoic acid, the first-discovered hepatocyte nuclear factor 4 alpha agonist, inhibits multistep liver carcinogenesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1904.

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WANG, Zhu, and Franky Leung Chan. "Abstract 4576: Hepatocyte nuclear factor 4 alpha suppresses cell proliferation and induces cellular senescence and apoptosis in prostate cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4576.

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Harrison, R. "HUMAN HEPATIC ENDOTHELIAL CELLS AND HEPATOCYTES IN CULTURE: MORPHOLOGICAL FEATURES, AND PRODUCTION OF VON WILLEBRAND FACTOR AND FIBRINOGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643350.

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Liver cells were derived from cadaveric organ donors. Pieces of human liver 5 to 50 grams were minced, washed, and incubated in collagenase at 37 degrees C. After washing, the cell suspension was plated into culture vessels that had been briefly pre-treated with an extract derived from human liver. A mixed population of liver cells, including endothelial cells, hepatocytes, and Kupffer cells, attached within hours. At the end of 2 to 3 weeks there developed clusters of densely packed cells of two types. The most numerous cells were initially fusiform but grew as a monolayer even when densely packed. As density increased they assumed a polygonal form; cells with this morphological appearance stained immunocytochemically for von Willebrand factor antigen. They were relatively small and resembled cells derived from human umbilical vein except that the cytoplasm was more filmy in appearance. The second prominent cell type was significantly larger and likewise replicated to form clusters. These large cells sometimes contained multiple nuclei, exhibited a relatively low nuclear to cytoplasmic ratio, and immunocytochemically stained for human fibrinogen. A more distinct nuclear membrane and prominent nucleoli were characteristics of hepatocytes that were useful light microscopically in distinguishing these cells from sinusoidal endothelial cells. Ultrastructurally, endothelial cells were characterized by small size, holes in and among the cells that probably were the in vitro analogue of fenestrae, and numerous Weibel-Palade bodies in the cytoplasm, which otherwise was relatively bland. Hepatocytes, by contrast, had an active appearing cytoplasm containing more organelles. Canaliculi and typical tight junctions formed between adjacent hepatocytes. Levels of vWF and fibrinogen increased in a time dependent manner in media overlying this mixed population of cells. Human factor VIII has not yet been detected in the media overlying these mixed cells derived from human liver, and factor VIII antigen has not yet been demonstrable immunocytochemically in either cell type.
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Reports on the topic "Hepatocyte nuclear factor"

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Mirosevich, Janni. Investigating the Role of Hepatocyte Nuclear Factor-3 (HNF-3) Alpha and Beta in Prostate Cancer and Cellular Differentiation. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada455964.

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Mirosevich, Janni. Investigating the Role of Hepatocyte Nuclear Factor-3 (HNF-3) Alpha and Beta in Prostate Cancer and Cellular Differentiation. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada431320.

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