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.
Full textBingham, 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.
Full textHannoun, Zara. "Role of SUMO modification in hepatocyte differentiation." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5917.
Full textChéret, 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.
Full textGresh, Lionel. "Rôles du facteur de transcription hepatocyte nuclear factor 1beta au cours de l'organogenèse." Paris 6, 2004. http://www.theses.fr/2004PA066143.
Full textChellappa, 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.
Full textIncludes abstract. Includes bibliographical references (leaves 293-348). Issued in print and online. Available via ProQuest Digital Dissertations.
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.
Full textPapachristodoulou, 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.
Full textXu, 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.
Full textKaratza, 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.
Full textStride, Amanda. "The phenotype of subjects with a mutation in the hepatocyte nuclear factor-1 alpha gene." Thesis, University of Exeter, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424848.
Full textXu, Jianyu, and 許健瑜. "Mutations in the hepatocyte nuclear factor 1 and glucokinase genes in Southern Chinese patients with early-onset type 2 diabetes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B42576854.
Full textTa, Tuong Chi. "The essential fatty acid linoleic acid is the endogenous ligand for the Orphan nuclear receptor Hepatocyte nuclear factor 4 Aplha." Diss., UC access only, 2009. http://proquest.umi.com/pqdweb?did=1871881951&sid=1&Fmt=7&clientId=48051&RQT=309&VName=PQD.
Full textDevonshire, Alison. "The role of hepatocyte nuclear factor 4α (HNF4α) in the metabolic regulation of its target genes." Thesis, University of Surrey, 2008. http://epubs.surrey.ac.uk/842743/.
Full textOkamoto, Takako. "Hepatocyte nuclear factor-1β (HNF-1β) promotes glucose uptake and glycolytic activity in ovarian clear cell carcinoma." Kyoto University, 2014. http://hdl.handle.net/2433/185193.
Full textKyoto University (京都大学)
0048
新制・論文博士
博士(医学)
乙第12804号
論医博第2076号
新制||医||1001(附属図書館)
80848
京都大学大学院医学研究科医学専攻
(主査)教授 野田 亮, 教授 武藤 学, 教授 稲垣 暢也
学位規則第4条第2項該当
Gardner-Stephen, Dione Anne, and dione bourne@flinders edu au. "Transcriptional Regulation of Human UDP-Glucuronosyltransferases." Flinders University. Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20081111.223136.
Full textCOFFINIER, CATHERINE. "Etude du profil d'expression et de l'inactivation du gene vhnf1 (variant hepatocyte nuclear factor 1) chez la souris." Paris 11, 1999. http://www.theses.fr/1999PA112104.
Full textNakajima, Naoki. "GATA6-positive lung adenocarcinomas are associated with invasive mucinous adenocarcinoma morphology, hepatocyte nuclear factor 4α expression, and KRAS mutations." Kyoto University, 2020. http://hdl.handle.net/2433/253168.
Full textBunaciu, Rodica Petruta. "THE EFFECT OF POLYCHLORINATED BIPHENYLS ON LIVER TUMOR PROMOTION: A ROLE FOR KUPFFER CELLS?" Lexington, Ky. : [University of Kentucky Libraries], 2005. http://lib.uky.edu/ETD/ukynusi2005d00298/etd.pdf.
Full textTitle from document title page (viewed on November 4, 2005). Document formatted into pages; contains viii, 188 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 165-184).
Briançon, Nadège. "Hepatocyte Nuclear Factor 4αʾ : régulation transcriptionnelle du promoteur distal et étude fonctionnelle des isoformes par "knock-in" réciproques chez la souris." Paris 6, 2005. http://www.theses.fr/2005PA066003.
Full textYu, Li. "Genetic variation in the hepatocyte nuclear factor (HNF)-3α gene does not contribute to maturity-onset diabetes of the young in Japanese." Kyoto University, 2003. http://hdl.handle.net/2433/148693.
Full textRen, Hui. "REGULATION OF HEPATIC GENE EXPRESSION DURING LIVER DEVELOPMENT AND DISEASE." UKnowledge, 2012. http://uknowledge.uky.edu/microbio_etds/6.
Full textArpiainen, S. (Satu). "Transcriptional regulation of the hepatic cytochrome P450 2a5 gene." Doctoral thesis, University of Oulu, 2007. http://urn.fi/urn:isbn:9789514285653.
Full textEleswarapu, Satyanarayana. "Mechanisms of Growth Hormone Regulation of Insulin-Like Growth Factor-I Gene Expression in Liver." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/37373.
Full textPh. D.
Chardès, Brieux. "Inhibition du Virus de l’Hépatite Delta par des inducteurs de la voie NFκB." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1141.
Full textSuper-infection by Hepatitis Delta Virus (HDV) of chronically Hepatitis B Virus (HBV) infected patients leads to the most aggressive forms of chronic viral hepatitis, with a faster progression towards fibrosis/cirrhosis and an increased risk of liver failure and hepatocellular carcinoma. Around 15-20 millions of people are co-infected with both viruses, which ranks this co-infection as one of the most prevalent and clinically challenging of the world. HDV infection is not susceptible to available direct anti-HBV. The only therapeutic option for HBV/HDV co-infected patients is the pegylated-interferon-α, a drug which has many side effects and suboptimal responses. Few molecules that target HDV are currently in development but none of them is affecting the replicative step of this virus. There is an urgent need to develop efficient treatment strategies for patients. An infection produced many cytokines. Different studies showed an activation of the interferon pathway during HDV infection in vitro and in vivo. Nevertheless, there is no current data available concerning an activation of the Nuclear factor κ B » (NFκB) pathway by HDV, and more than that our laboratory has suggested a lack of activation. Our purpose was to test the effect on HDV of various immunomodulatory drugs activating this pathway. After screening of various inducers of the canonical and non-canonical NFκB pathways we identified an agonist of the “toll like” receptor 1/2 (Pam3CSK4) and an agonist of the lymphotoxin β receptor (BS1) decreasing the HDV RNA and proteins. More extensive studies have shown a dose-dependent and stable anti-HDV effect despite an increase of the number of viral particles used to infect cells. Rebound experiments have shown a persistent antiviral effect and an alteration of the HDV particles infectivity. Its suggests an irreversible effect on HDV replication and transcription template. Transcriptomic analysis on HBV/HDV infected and treated with Pam3CSK4 and BS1 cells has confirmed the induction of the NFκB pathway and revealed the activation of numerous genes involved in an inflammatory response. A Gene Ontology study of molecular functions and cellular processes significantly modulated by Pam3CSK4 or BS1 treatments had enable us to identify a list of potential effectors targeting the RNA and responsible of the anti-HDV phenotype. The underlying mechanism (i.e. RNA degradation or negative regulation of transcription) remains to be deciphered. Our project has shown that the NFκB induction is a potential target to inhibit the HDV infection. Research of effector(s) will probably enable us to identify a new restriction factor. Thus, our research efforts should pave the way for the development of novel efficient antiviral strategies to eliminate HDV
Rocha, Tatiana Marques Ferreira da. "Associação entre polimorfismos nos genes SLC2A1, SLC2A2, HNF1A, TGFB1 e DCP1A e nefropatia em portadores de diabetes mellitus tipo 1." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-26032013-141528/.
Full textDiabetic nephropathy (DN) results from chronic hyperglycemia, risk factors such as hypertension and dyslipidemia as well as from genetic susceptibility, already demonstrated in numerous clinical studies. A histological feature of DN is the accumulation of extracellular matrix proteins in the mesangium after activation of multiple biochemical pathways. GLUT-1, encoded by gene SLC2A1, is the major glucose transporter in mesangial cell and its expression is increased in the glomeruli of diabetic animals, comprising a positive feedback loop whereby high extracellular glucose stimulates its own uptake and worsening mesangial injury. GLUT-2, encoded by SLC2A2 gene, is expressed in podocytes and tubular cells and its expression is also increased in DN. The expression of this glucose transporter is regulated by the transcription factor HNF-1. Transforming growth factor - (TGF-) also participates in renal injury induced by hyperglycemia, exerting several deleterious effects, such as to decrease the activity of matrix metalloproteinases and to promote renal fibrosis. This growth factor determines the transcriptional activation of target genes, but needs other activators and co-activators, such as the protein named SMIF, encoded by the gene DCP1A. Given the involvement of the aforementioned proteins in the pathogenesis of DN, the present study aimed to evaluate the association of single nucleotide polymorphisms (SNPs) in the genes SLC2A1, SLC2A2, HNF1A, TGFB1 e DCP1A with renal disease in patients with type 1 diabetes mellitus (T1DM). A total of 449 patients (56.4% female, mean age 36.0±11.0 years) with disease duration > 10 years were included and grouped according to DN stages: (1) absence of DN: normal urinary albumin excretion (UAE) (< 30 mg/24h or < 20 g/min) and plasmatic creatinine < 1.7 mg/dL without antihypertensive treatment; (2) incipient DN: microalbuminuria (UAE 30 299 mg/24h or 20 199 g/min) and plasmatic creatinine < 1.7 mg/dL without antihypertensive treatment and (3) overt DN: macroalbuminúria (UAE > 300 mg/24h or > 200 g/min) or proteinuria or renal replacement therapy. Associations of SNPs with estimated glomerular filtration rate (eGFR) were also evaluated. All SNPs were genotyped by real time polymerase chain reaction using fluorescent-labelled probes. Associations of the SNPs with DN were assessed by logistic regression analyses and odds ratios (OR) were calculated after adjustments for possible confounders included as covariables in the regressive model. P values <0.05 (two-tails) were considered significant. The following associations were observed: (1) SLC2A1: genotypes CT+TT from rs841848 conferred risk to incipient DN in the overall population (OR 1.88; 95%IC 1.06-3.34; P= 0.03) and in the male patients (OR 2.67; CI95% 1.13-6.35; P=0.0247) and to overt DN (OR 2.70; CI95% 1.18-6.31; e P= 0.0197) only in the male patients; genotypes GA+AA from rs1385129 conferred risk to overt DN in the male population (OR 3.09; CI95% 1.34-7.25; P=0.0085); genotypes AT + TT from rs3820589 conferred protection against incipient DN in the overall population (OR 0.36; CI95% 0.16-0.78; P=0.0132) and in the female population (OR 0.14; CI95% 0.02-0.52; P=0.0122). (2) SLC2A2: genotypes GA+GG from rs5396 conferred protection against overt DN in the male patients (OR 0.29; CI95% 0.12-0.69; P=0.0052); genotypes AG+GG from rs6800180 conferred protection against overt DN in the male patients (OR 0.16; CI95% 0.14-0.90; P=0.0324). (3) HNF1A: genotypes AC + CC from rs1169288 conferred risk to overt DN in the overall population (OR 2.23; CI95% 1.16-4.38; P=0.0175); genotypes CG+GG from rs1169289 conferred risk to overt DN in the overall population (OR 3.43; CI95% 1.61-7.73; P=0.002); (4) TGFB1: genotypes CT + TT from 1800468 conferred risk to incipient DN in the overall population (OR 2.99; CI95% 1.26-7.02; P=0.0116) and the polymorphic allele T from SNP rs1800469 conferred risk to a lower eGFR (p=0.0271). (5) DCP1A: the polymorphic allele A from SNP rs11925433 was also associated with a lower eGFR (p=0.0075). In conclusion, SNPs in the genes encoding proteins GLUT-1, GLUT-2, HNF-1, TGF- e SMIF, all involved in the pathogenesis of DN, conferred susceptibility to this chronic complication in the T1DM patients evaluated in the present study
Lee, Sihyi, and 李思怡. "Functional Analysis of Tilapia (Oreochromis mossambicus) Hepatocyte Nuclear Factor-3β Promoter Fragments." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/67540607462477019848.
Full text大葉大學
分子生物科技學系碩士班
100
The hepatocyte nuclear factors-3 (HNF-3) family members HNF-3α, HNF-3β and HNF-3γ are hepatocyte-enriched transcription factors, they play important roles in controlling development, differentiation, metabolism and organogenesis. In our previous study, the expression of insulin-like growth factor-I/II (IGF-I/II), HNF-1α, -1β and -3β were detected in the liver and gonads of tilapia, and expreession level of HNF-3β was higher than others and it could be regulated by 17β-estradiol. In this study, four fragments (0.5, 1.0, 1.5 and 2.0 kb) of tilapia HNF-3β promoter were constructed with green fluorescent protein (GFP) gene for biological activity assay by performing transfection into tilapia ovarian cell line (TO-2) and human hepatoma cell line (Hep3B) for western blot analysis and luciferase assay or microinjection into zebrafish eggs and assay. The GFP was mainly expressed in yolk and somites 24 h after injection, in notochord and floor plate 96 h after injection. The 0.5 kb fragment was expressed in notochord, yolk, eye and head, the expression rates were 18.3%, 1.3%, 35.6% and 26.0%, respectively; the 1.0 kb fragment was expressed in notochord, yolk, and head, the expression rates were 44.4%, 44.4% and 2.0%, respectively; the 1.5 kb fragment was expressed in notochord and yolk, the expression rates were 33.7% and 50.5% respectively, and the 2.0 kb fragment was expressed in notochord, yolk and head, the expression rates were 61.2%, 26.1% and 2.7% respectively. The results were similar to our previous studies. The supplement of add 17β-estradiol enhanced western blot analysis of eGFP expression and luciferase assay in TO-2 and Hep3B cells. Based on the present results, hypothesizing that estrogen response element (ERE) in tilapia HNF-3β promoter could promote the expression of HNF-3β in the gonads of tilapia through the action of steroids.
Krajewski, Jochen Christian [Verfasser]. "Die Bedeutung des Transkriptions-hepatocyte-nuclear-factor-4α [Transkriptions-hepatocyte-nuclear-factor-4-alpha] für die Repression des Erythropoietin-Gens durch {Interleukin-1β [Interleukin-1-beta] / vorgelegt von Jochen Christian Krajewski." 2006. http://d-nb.info/984150412/34.
Full textChih-Chien, Hsu, and 許志堅. "Molecular Cloning and Localization of The Tilapia (Oreochromis mossambicus)Hepatocyte Nuclear Factor (HNF)-4a." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/14789305249316826974.
Full text大葉大學
分子生物科技學系碩士班
94
Hepatocyte nuclear factor (HNF)-4 is a liver-enriched transcription factor and belongs to the highly conserved member of the nuclear receptor superfamily. HNF-4 together with other factors play a key role in the tissue specific expression of a large number of genes involved in lipid and glucose metabolism. However, its function in fish is still poorly understood. In our previous study, RNAs and proteins of HNF-1, HNF-1, and HNF-3are detected in the liver, ovary, and testis of tilapia (Oreochromis mossambicus). And the expression of HNF-3 in the gonads could be induced by 17-estradiol and hydrocortisone in vitro. Besides, HNF-4 binding site on the promoter region of HNF-3 gene has also been found. However, there are only limited literatures dealing with HNFs in bony fish. The roles and their relation of HNFs in the physiology of fish remain to be explored. Here we report on the first cloning of full-length cDNA and protein localization of HNF-4from a tilapia (O. mossambicus). A total of 2,031 bp of tilapia HNF-4fhas been cloned and its deduced amino acid sequence of the coding region (340 amino acids) of tilapia HNF-4 has a 89% identity with that of zebrafish, over 84% with mammals (human, bovine, rat, and mouse), 81% with chicken, and 79% with Xenopus. RT-PCR detected HNF-4in liver, kidney, intestine and stomach, and the identity of the PCR fragments was confirmed by sequencing analysis and PCR hybridization. Its relative expression ratio was higher in the liver than in intestine and kidney, and lowest expression ratio was observed in stomach. The same result happened in both genders. Western blotting and immunohistochemical localization also detected HNF-4 protein in the tissues mentioned before. Expression of HNF-4 in the tilapia suggests that multi-HNFs may form a cascade to regulate physiology in the bony fish.
Chen, Hue-Ling, and 陳惠玲. "The Cloning and Regulatory Analysis of Tilapia (Oreochromis mossambicus) Hepatocyte Nuclear Factor-3b Promoter." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/22124471280928720560.
Full text大葉大學
分子生物科技學系碩士班
94
The hepatocyte nuclear factors-3 (HNF-3) family members HNF-3, HNF-3 and HNF-3 are hepatocyte-enriched transcription factors, they play important roles in controlling development, cell differentiation, organogenesis and in the regulation of metabolism. In our previous study, the expression of insulin-like growth factor-I (IGF-I), IGF-II, HNF-1a, -1b, and -3bwere detected in the liver and gonads of tilapia, and the expression level of HNF-3b was higher than others and it could be regulated by 17b-estradiol. Based on the results, the aim of this study was to clone and analyze the tilapia HNF-3b promoter, and to provide a foundation for further studies on the relation between HNFs and gonad/gamete development in tilapia, and on biomedical and developmental studies in the future. The 5’-flanking region of tilapia HNF-3b promoter containing 2364 bp was cloned and sequenced, and on which 373 putative transcription factor binding sites for HNFs (HNF-1, -3, -4 and -6), CCAAT/enhancer binding protein(C/EBP), cAMP responsive element binding (CREB), sterol regulatory element, steroid hormones receptor binding site, signal transducer and activator of transcription (STAT), GATA-binding factor and other factors were found. These factors are important for embryo development and gonadal function. Four deletion fragments (2, 1,5, 1 and 0.5 kb) of tilapia HNF-3b promoter were constructed with green fluorescent protein (GFP) gene for biological activity assay by cell line (TO-2 and Hep3B) transfection or microinjection into zebrafish eggs. The GFP was mainly expressed in yolk and somite 10 h after injection, and in somite, notochord and floor plate 72 h after injection, but that of 0.5 kb fragment was mainly expressed in eye and head. And the expression rates of 2 kb and 1.5 kb groups seemed better than those of 1 kb and 0.5 kb (p<0.05). Western blotting analysis of GFP expression in TO-2 and Hep3B cells after transfected with different of tilapia HNF-3b promoter proximal regions showed that 1 kb proximal region had a lower expression level than others (2, 1.5, 0.5 kb), this could result from the repressor binding site on the 1 kb region. The effect of steroid hormones (17b-estradiol and progesterone) on the expression of GFP after injection or transfection of the 4 fragments into zebrafish eggs or cells showed the level of GFP expression of these groups increased significantly. Based on the present results, hypothesizing that estrogen response element (ERE) and progesterone receptor region in tilapia HNF-3b promoter could promote the expression of HNF-3b in the gonads of tilapia through the action of steroids, however, the actual mechanism needs further study.
Hsu, Yu-Hua, and 許育華. "Regulation of hepatocyte nuclear factor 4 alpha (HNF4α) expression in hepatocellular carcinoma cell lines." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/51626457187763530687.
Full text慈濟大學
人類遺傳研究所
94
It has been reported that in mouse hepatogenesis HNF4α is essential for the expression of E-cadherin in the organ formation. Thus if HNF4α is down-regulated the consequence would be the lost of polarity and increase in cell mobility and invasiveness of hepatocyte. Whether HNF4α can regulate metastasis of human hepatoma cell has not been determined yet. It has been reported that in most hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) SMYD3, a histone methyaltranferase, was over expressed. SMYD3 can down-regulate HNF4α. The decreased HNF4αexpression may alter carcinogenesis of HCC through decrease expression of E-cadherin, thus increasing metastatic potential of HCC. The aim of this study is to characterize several transcription factors (TFs) that are important in regulating HNF4α expression in the HCC. Here, we examined whether deletions of SMYD3 binding motif in the promoter region of HNF4αcould increase the metastasis potential of human hepatoma cell lines. The results of functional assay of SMYD3 on HNF4α regulatory sequence could not confirm the previous study. Therefore SMYD3 appeared not to be a critical factor for HNF4α expression in our study. More detailed serial deletions of HNF4αpromoter allowed us to identify three putative positive regulatory elements and one putative negative regulatory element. We want to identify which transcription factor acts as a positive modulator for the HNF4αexpression. There are two putative SP1 binding motifs in the HNF4α promoter region at (-243/154) and (-192/154), respectively. The results of functional assays indicated that SP1 binding motif in the (-192/154) promoter region may not be functional. The functional SP1 binding motif is located in the position of -243. Our results also showed that Cdx2A is a negative regulator for HNF4α, thus it may be a potential suppressor for E-cadherin expression, it may also contribute to HCC metastasis.
Yu, Hao-Cheng, and 余浩成. "Studies on the Tilapia (Oreochromis mossambicus) Hepatocyte Nuclear Factor-1 and -3 in the Regulation of Reproductive System." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/23254843122837346213.
Full text大葉大學
分子生物科技學系碩士班
93
Tilapia is the most general aguacultivating fish in the fresh water and has characteristics of fast growing and well disease resistance. Thus tilapia is an important animal model for relative aquaculture researches. Hepatocyte nuclear factors (HNFs) are liver-enriched transcription factors, which can activate the expressions of tissue-specific, growth and development related genes. The expression of HNFs was detected in the gonads of tilapia previously, and which could be regulated by steroid hormones. Therefore, the reproductive system in tilapia could exist a different endocrine pathway other than the traditional one. To identify this hypothesis and to find out the optimal steroid, concentration and culture period, gonads from tilapia were cultured in vitro in a time course manner (0, 6, 12, 18, 24, 32 and 36 hrs) with different kinds (-estradiol and hydrocortisone) or concentrations (0, 0.1, 1, 10, 100 and 1000 nM) of steroid hormones, which were all performed after a 6-hr preculture without hormone supplement. The total RNA isolated from previous different groups was analyzed by RT-PCR and semi-quantified with an internal control of -actin. Though the expression of HNF-1 and -1 could not be induced by -estradiol and hydrocortisone, the expression of HNF-3 could be induced by these two steroids, and showed a dose-dependent manner. Beta-estradiol exerted a better induction result, and the optimal concentration and incubation period were 10 nM and 12 hours, respectively. The detection of HNF proteins in 1-, 2-week and one month old juvenile tilapia by immunohistochemistry showed that HNFs were found mainly in liver and epithelial cells of the digestive organs. According to the above results, the expression of HNF-3β in the gonads of tilapia can be regulated by the steroid hormone and could be involved in the development and gametogenesis of gonads in tilapia. Whether the growth and development of juvenile tilapia is affected by HNFs still needs further investigation.
Cliff, Ji-Fan Lin, and 林致凡. "Two Isoforms of Hepatocyte Nuclear Factor 1-alpha (HNF1-alpha) in Tilapia (Oreochromis mossambicus) Which Transactivate IGF-I Gene Expression." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/79388460468221975578.
Full text國立海洋大學
水產生物技術研究所
87
The liver-enriched hepatocyte nuclear factor 1 (HNF1) is an important transcription factor for IGF-I in adult liver. Only one conserved HNF1 binding site was found near the transcription initiation site of tilapia IGF-I gene. To study the role of HNF1 in the signaling pathway of GH-IGF-I axis, degenerated primers designed from known sequences of HNF1 were used to amplify HNF1 partial sequence from tilapia liver mRNA by one step RT-PCR. After gel electrophoresis, RT-PCR product revealed two major bands in size of 400 and 500 bps. Sequence comparisons of these 400 bps and 500 bps clones showed highly homologous to HNF1-alpha and HNF1-beta, respectively. Furthermore, comparison of POU and homeo-domain within HNF1-alpha (400 bps) clones, we found two types of HNF1-alpha with four amino acids variation in the C-terminal of homeo-domain. One is highly homologous to salmon HNF1 and the other is similar to mammalian HNF1-alpha in amino acid usage. This is the first evidence to show HNF1-beta existing in fish and two different types of HNF1-alpha observed in vertebrates. Both HNF1-alpha and HNF1-betacDNA clones with 5’-truncation were obtained from tilapia liver cDNA library, and 5’RACE then was applied to amplify the 5’ truncated region of HNF1-alpha cDNA. Full length HNF1-alpha cDNA was re-amplified by using 5’ and 3’primer located at the terminal of its ORF. Two HNF1-alpha full-length cDNAs in length of 1680 and 1760 bps were obtained and designated as tiHNF1-alpha-A and tiHNF1-alpha-B, respectively. Compared with other known HNF1s, the dimerization domain, POU domain and homeo-domain of tiHNF1-alpha-A consisting of 559 amino acids were highly conserved. tiHNF1-alpha-B had a 80bp insertion containing an in-frame stop codon, and this insert replaced the last 107 amino acids of the tiHNF1-alpha-A protein with 6 amino acids resulting in a 458 amino acids protein. In vitro transcription and translation was carried out to verify the different protein size of these two clones. Sequence comparisons of tiHNF1-alpha-A with human HNF1-A and B suggest that close related mechanism of alternative splicing results in the occurrence of tiHNF1-alpha-B. Different sizes of PCR amplified tilapia IGF-I promoters were constructed into luciferase reporter vector for further studies on the binding and transactivation ability of tilapia HNF1s.
Michaud, Josée. "L’inhibition des cytochromes P450 dans les cas d’insuffisance rénale chronique : rôle de l’hormone parathyroïdienne." Thèse, 2012. http://hdl.handle.net/1866/10228.
Full text