Relevant bibliographies by topics / Hepatocyte-Nuclear-Factor -1-A (HNF1A)

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Academic literature on the topic 'Hepatocyte-Nuclear-Factor -1-A (HNF1A)'

Author: Grafiati
Published: 15 June 2024
Last updated: 31 July 2025

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Journal articles on the topic "Hepatocyte-Nuclear-Factor -1-A (HNF1A)"

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Mehdi, Alina Z., Lily Deng, Colby L. Chase, et al. "GLP-1 RA and dual GIP/GLP-1 RA treatment in MODY: a descriptive case series." BMJ Open Diabetes Research & Care 13, no. 2 (2025): e004885. https://doi.org/10.1136/bmjdrc-2024-004885.

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IntroductionGlucagon-like peptide-1 receptor agonists (GLP-1 RA) and dual glucose insulinotropic polypeptide (GIP)/GLP-1 RA are widely prescribed, but their effectiveness in different subtypes of maturity-onset diabetes of the young (MODY) is unknown.Research design and methodsWe present a descriptive case series of individuals from two MODY cohorts who used GLP-1 RA or dual GIP/GLP-1 RA. Pairedttests were used to compare HbA1c, body mass index (BMI), and sulfonylurea (SU) dose before and after GLP-1 RA or dual GIP/GLP-1 RA therapy.Results10 individuals (4 hepatocyte nuclear factor-1α (HNF1A)-
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Ozsu, Elif, Filiz Mine Cizmecioglu, Gul Yesiltepe Mutlu, et al. "Maturity Onset Diabetes of the Young due to Glucokinase, HNF1-A, HNF1-B, and HNF4-A Mutations in a Cohort of Turkish Children Diagnosed as Type 1 Diabetes Mellitus." Hormone Research in Paediatrics 90, no. 4 (2018): 257–65. http://dx.doi.org/10.1159/000494431.

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Background/Aims: Maturity onset diabetes of the young (MODY) is a rare condition often misdiagnosed as type 1 diabetes (T1D). The purposes of this study were: to identify any patients followed in a large Turkish cohort as T1D, with an atypical natural history, who may in fact have MODY, and to define the criteria which would indicate patients with likely MODY as early as possible after presentation to allow prompt genetic testing. Methods: Urinary C-peptide/creatinine ratio (UCPCR) was studied in 152 patients having a diagnosis of T1D for at least 3 years. Those with a UCPCR ≥0.2 nmol/mmol wer
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Au, Wo-Shing, Liwei Lu, Chung-Man Yeung, et al. "Hepatocyte nuclear factor 1 binding element within the promoter of microsomal triglyceride transfer protein (MTTP) gene is crucial for MTTP basal expression and insulin responsiveness." Journal of Molecular Endocrinology 41, no. 4 (2008): 229–38. http://dx.doi.org/10.1677/jme-08-0080.

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Insulin inhibits the transcription of the microsomal triglyceride transfer protein (MTTP), which plays a pivotal role in lipoprotein assembly and secretion. Here, we provide evidence that a hepatocyte nuclear factor 1 binding element (HNF1A element) within the MTTP promoter serves as a novel negative insulin-responsive element. Deletion/mutation mapping of the MTTP gene promoter identified a modified HNF1A element that is crucial to the negative insulin effect. Chimeric promoter containing this HNF1A element and minimal TEAD1 promoter also responded negatively toward insulin treatment. Gel shi
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Tudor, Lucija, Marcela Konjevod, Gordana Nedic Erjavec та ін. "Genetic and Epigenetic Association of Hepatocyte Nuclear Factor-1α with Glycosylation in Post-Traumatic Stress Disorder". Genes 13, № 6 (2022): 1063. http://dx.doi.org/10.3390/genes13061063.

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Post-traumatic stress disorder (PTSD) is a complex trauma-related disorder, the etiology and underlying molecular mechanisms of which are still unclear and probably involve different (epi)genetic and environmental factors. Protein N-glycosylation is a common post-translational modification that has been associated with several pathophysiological states, including inflammation and PTSD. Hepatocyte nuclear factor-1α (HNF1A) is a transcriptional regulator of many genes involved in the inflammatory processes, and it has been identified as master regulator of plasma protein glycosylation. The aim o
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Bonzo, Jessica A., Andrew D. Patterson, Kristopher W. Krausz та Frank J. Gonzalez. "Metabolomics Identifies Novel Hnf1α-Dependent Physiological Pathways in Vivo". Molecular Endocrinology 24, № 12 (2010): 2343–55. http://dx.doi.org/10.1210/me.2010-0130.

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Abstract Mutations in the HNF1A gene cause maturity-onset diabetes of the young type 3, one of the most common genetic causes of non-insulin-dependent (type 2) diabetes mellitus. Although the whole-body Hnf1a-null mouse recapitulates the low insulin levels and high blood glucose observed in human maturity-onset diabetes of the young type 3 patients, these mice also suffer from Laron dwarfism and aminoaciduria, suggesting a role for hepatocyte nuclear factor 1α (Hnf1α) in pathophysiologies distinct from non-insulin-dependent (type 2) diabetes mellitus. In an effort to identify pathways associat
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Chen, Yinling, Jianxin Jia, Qing Zhao та ін. "Novel Loss-of-Function Variant in HNF1a Induces β-Cell Dysfunction through Endoplasmic Reticulum Stress". International Journal of Molecular Sciences 23, № 21 (2022): 13022. http://dx.doi.org/10.3390/ijms232113022.

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Heterozygous variants in the hepatocyte nuclear factor 1a (HNF1a) cause MODY3 (maturity-onset diabetes of the young, type 3). In this study, we found a case of novel HNF1a p.Gln125* (HNF1a-Q125ter) variant clinically. However, the molecular mechanism linking the new HNF1a variant to impaired islet β-cell function remains unclear. Firstly, a similar HNF1a-Q125ter variant in zebrafish (hnf1a+/−) was generated by CRISPR/Cas9. We further crossed hnf1a+/− with several zebrafish reporter lines to investigate pancreatic β-cell function. Next, we introduced HNF1a-Q125ter and HNF1a shRNA plasmids into
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Liu, Rui, Hanning Liu, Haiyong Gu, et al. "A Polymorphism inHepatocyte Nuclear Factor 1 Alpha,rs7310409, Is Associated with Left Main Coronary Artery Disease." Biochemistry Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/924105.

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Coronary artery disease is the leading cause of mortality and morbidity in the world. Left main coronary artery disease (LMCAD) is a particularly severe phenotypic form of CAD and has a genetic basis. We hypothesized that some inflammation- and hyperhomocysteinemia-related gene polymorphisms may contribute to LMCAD susceptibility in a Chinese population. We studied the association between polymorphisms in the genes hepatocyte nuclear factor 1 alpha (HNF1A; rs7310409, G/A), C-reactive protein (rs1800947 and rs3093059 T/C), methylenetetrahydrofolate reductase (rs1801133, C/T), and methylenetetra
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Demus, Daniel, Paulina A. Urbanowicz, Richard A. Gardner та ін. "Development of an exoglycosidase plate-based assay for detecting α1-3,4 fucosylation biomarker in individuals with HNF1A-MODY". Glycobiology 32, № 3 (2021): 230–38. http://dx.doi.org/10.1093/glycob/cwab107.

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Abstract Maturity-onset diabetes of the young due to hepatocyte nuclear factor-1 alpha variants (HNF1A-MODY) causes monogenic diabetes. Individuals carrying damaging variants in HNF1A show decreased levels of α1-3,4 fucosylation, as demonstrated on antennary fucosylation of blood plasma N-glycans. The excellent diagnostic performance of this glycan biomarker in blood plasma N-glycans of individuals with HNF1A-MODY has been demonstrated using liquid chromatography methods. Here, we have developed a high-throughput exoglycosidase plate-based assay to measure α1-3,4 fucosylation levels in blood p
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9

Dallali, Hamza, Meriem Hechmi, Imane Morjane, et al. "Association of HNF1A gene variants and haplotypes with metabolic syndrome: a case–control study in the Tunisian population and a meta-analysis." Diabetology & Metabolic Syndrome 14, no. 1 (2022): 25. https://doi.org/10.1186/s13098-022-00794-0.

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<strong>Background: </strong>Variants in the Hepatocyte Nuclear Factor 1 Alpha gene (<i>HNF1A</i>) are associated with lipoproteins levels and type 2 diabetes. In this study, we aimed to assess the association of <i>HNF1A</i> gene and haplotypes with the metabolic syndrome (MetS) and its components through an association study in the Tunisian population as well as by a meta-analysis.<strong>Methods: </strong>A total of 594 Tunisian individuals were genotyped for three variants (rs1169288, rs2464196 and rs735396) located in <i>HNF1A</i> gene using KASPar technology. Statistical analyses were pe
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Ma, Yumin, Siqian Gong, Xirui Wang, et al. "New clinical screening strategy to distinguish HNF1A variant-induced diabetes from young early-onset type 2 diabetes in a Chinese population." BMJ Open Diabetes Research & Care 8, no. 1 (2020): e000745. http://dx.doi.org/10.1136/bmjdrc-2019-000745.

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ObjectiveMaturity-onset diabetes of the young caused by hepatocyte nuclear factor-1 alpha (HNF1A) variants (HNF1A-MODY) is a common form of monogenetic diabetes. Although patients with HNF1A-MODY might specifically benefit from sulfonylurea treatment, available methods for screening this specific type of diabetes are not cost-effective. This study was designed to establish an optimized clinical strategy based on multiple biomarkers to distinguish patients with HNF1A-MODY from clinically diagnosed early-onset type 2 diabetes (EOD) for genetic testing in a Chinese population.Research design and
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Dissertations / Theses on the topic "Hepatocyte-Nuclear-Factor -1-A (HNF1A)"

1

Acosta, Montalvo Ana. "The Role of Hepatocyte-Nuclear-Factor-1-A (HNF1A) in the Regulation of Glucose Homeostasis and Pancreatic Hormone Secretion." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS043.

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Le Hepatocyte-nuclear-factor-1-alpha (HNF1A) est un facteur de transcription clé qui régule l'expression de nombreux gènes impliqués dans plusieurs processus métaboliques, notamment dans le foie, l'intestin, le rein et le pancréas. Les mutations hétérozygotes du gène HNF1A sont à l'origine de la forme la plus fréquente de diabète monogénique appelée "Maturity-onset-diabetes-of-the-young" (MODY),communément appelée HNF1A-MODY. Les porteurs de la mutation HNF1A-MODYdéveloppent une légère hyperglycémie dans l'enfance et un diabète plus tard dans la vie en raison d'une perte progressive de la fonc
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