Academic literature on the topic 'Hepatocyte-Nuclear-Factor -1-A (HNF1A)'
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Journal articles on the topic "Hepatocyte-Nuclear-Factor -1-A (HNF1A)":
Ozsu, Elif, Filiz Mine Cizmecioglu, Gul Yesiltepe Mutlu, Aysegul Bute Yuksel, Mursel Calıskan, Ahmet Yesilyurt, and Sukru Hatun. "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.
Au, Wo-Shing, Liwei Lu, Chung-Man Yeung, Ching-Chiu Liu, Oscar G. Wong, Lihui Lai, Hsiang-fu Kung, and Marie C. Lin. "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 (August 12, 2008): 229–38. http://dx.doi.org/10.1677/jme-08-0080.
Tudor, Lucija, Marcela Konjevod, Gordana Nedic Erjavec, Matea Nikolac Perkovic, Suzana Uzun, Oliver Kozumplik, Vlatka Zoldos, Gordan Lauc, Dubravka Svob Strac, and Nela Pivac. "Genetic and Epigenetic Association of Hepatocyte Nuclear Factor-1α with Glycosylation in Post-Traumatic Stress Disorder." Genes 13, no. 6 (June 14, 2022): 1063. http://dx.doi.org/10.3390/genes13061063.
Bonzo, Jessica A., Andrew D. Patterson, Kristopher W. Krausz, and Frank J. Gonzalez. "Metabolomics Identifies Novel Hnf1α-Dependent Physiological Pathways in Vivo." Molecular Endocrinology 24, no. 12 (December 1, 2010): 2343–55. http://dx.doi.org/10.1210/me.2010-0130.
Chen, Yinling, Jianxin Jia, Qing Zhao, Yuxian Zhang, Bingkun Huang, Likun Wang, Juanjuan Tian, Caoxin Huang, Mingyu Li, and Xuejun Li. "Novel Loss-of-Function Variant in HNF1a Induces β-Cell Dysfunction through Endoplasmic Reticulum Stress." International Journal of Molecular Sciences 23, no. 21 (October 27, 2022): 13022. http://dx.doi.org/10.3390/ijms232113022.
Liu, Rui, Hanning Liu, Haiyong Gu, Xiao Teng, Yu Nie, Zhou Zhou, Yan Zhao, Shengshou Hu, and Zhe Zheng. "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.
Demus, Daniel, Paulina A. Urbanowicz, Richard A. Gardner, Haiyang Wu, Agata Juszczak, Tamara Štambuk, Edita Pape Medvidović, et al. "Development of an exoglycosidase plate-based assay for detecting α1-3,4 fucosylation biomarker in individuals with HNF1A-MODY." Glycobiology 32, no. 3 (October 25, 2021): 230–38. http://dx.doi.org/10.1093/glycob/cwab107.
Ma, Yumin, Siqian Gong, Xirui Wang, Xiaoling Cai, Xinhua Xiao, Weijun Gu, Jinkui Yang, 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 (March 2020): e000745. http://dx.doi.org/10.1136/bmjdrc-2019-000745.
Pace, Nikolai Paul, Christopher Rizzo, Alexia Abela, Mark Gruppetta, Stephen Fava, Alex Felice, and Josanne Vassallo. "Identification of an HNF1A p.Gly292fs Frameshift Mutation Presenting as Diabetes During Pregnancy in a Maltese Family." Clinical Medicine Insights: Case Reports 12 (January 2019): 117954761983103. http://dx.doi.org/10.1177/1179547619831034.
Zhang, Chuanhui, Fei Xie, Ling Li, Cheng Zhang, Yong Zhang, Wantao Ying, Li Liu, Xuli Yan, Futao Yin, and Lianwen Zhang. "Hepatocyte nuclear factor 1 alpha (HNF1A) regulates transcription of O ‐GlcNAc transferase in a negative feedback mechanism." FEBS Letters 593, no. 10 (May 2019): 1050–60. http://dx.doi.org/10.1002/1873-3468.13381.
Dissertations / Theses on the topic "Hepatocyte-Nuclear-Factor -1-A (HNF1A)":
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.
Hepatocyte-nuclear-factor-1-alpha (HNF1A) is a key transcription factor that regulates the expression of numerous genes involved in several metabolic processes such as in the liver, intestine, kidney, and pancreas. Heterozygous mutations in the HNF1A gene causes the most frequent form of monogenic diabetes called Maturity-onset-diabetes-of-the-young (MODY), commonly referred to as HNF1A-MODY. HNF1A-MODY mutation carriers develop mild-hyperglycemia in childhood and diabetes later in life due to a progressive loss of beta cell function. However, since HNF1A is not only expressed in pancreatic beta cells, but also in alpha and delta cells, this thesis project was carried out to study the effect of HNF1A deficiency on intra-islet paracrine secretion, accompanied by alterations in genes encoding proteins that control glucose uptake and metabolism. To do so, I used cellular and mouse models of HNF1A-MODYdiabetes.The first cellular model I used was the beta-cell-derived rat insulinoma INS-1 cell line to conditionally overexpress the frameshift P291fsinsC mutation in the HNF1A gene(HNF1A-P291fsinsC), using a reverse tetracycline-dependent transactivator system. The expression of the P291fsinsC mutant protein was maximally induced to a significant level over that of endogenous Hnf1a by treating the cells with 500 ng/ml of doxycycline for (2 to 72 hrs). Non-induced INS-1 cells served as a control. Since INS-1 cells were previously reported to be bi-hormonal and did not express alpha cellmarkers, I utilized this model to study the effect of the HNF1A-P291fsinsC mutation on insulin and glucagon gene and protein expression and secretion. Cytometric and immunofluorescence analysis revealed that INS-1 cells comprised mostly of insulinpositivecells, whereas only a few cells co-expressed insulin and glucagon. However,both mature and immature beta cells secreted insulin and glucagon in response to glucose stimulation. Moreover, the overexpression of the HNF1A-P291fsinsC mutant protein increased proglucagon-derived peptide expression and glucagon secretion inresponse to high-glucose stimulation compared to non-induced INS-1 cells. These findings suggest that Hnf1A is essential to maintain beta cell maturation and function.Although INS-1 cells are a valuable tool to study beta-cell function, they do not resemble human islet cells in terms of paracrine signaling. Therefore, I developed an in vitro model by transfecting human islets with siRNAs targeting HNF1A (siHNF1A). I used islets deficient in HNF1A to investigate its effects on glucose transport and hormone secretion, simultaneously from the same donor islet preparations. siHNF1A transfections significantly decreased HNF1A protein levels compared to scrambled controls, observed by Western Blot analysis. siHNF1A also reduced insulin protein expression and secretion in response to high-glucose stimulation. This coincided with reduction in SGLT2 protein levels, with no changes in SGLT1, but a slight decrease inGLUT2. The decrease in SGLT2 was also associated with a significant increase inglucagon protein expression and secretion. These findings highlighted that HNF1A is also a key regulator of alpha cell function.Two HNF1A-MODY mouse models have previously been developed to study the pathogenesis of HNF1A-MODY in vivo. The first was a global Hnf1a-/- knock-out (KO) mouse and the second was a transgenic mouse that overexpresses the dominant-negative human mutant protein specifically in pancreatic beta cells, under the rat insulin promoter [...]