Relevant bibliographies by topics / G6PC

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'G6PC'

Author: Grafiati
Published: 2 September 2021
Last updated: 29 July 2025

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Journal articles on the topic "G6PC"

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Bosma, Karin J., Mohsin Rahim, Kritika Singh, et al. "Pancreatic islet beta cell-specific deletion of G6pc2 reduces fasting blood glucose." Journal of Molecular Endocrinology 64, no. 4 (2020): 235–48. http://dx.doi.org/10.1530/jme-20-0031.

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The G6PC1, G6PC2 and G6PC3 genes encode distinct glucose-6-phosphatase catalytic subunit (G6PC) isoforms. In mice, germline deletion of G6pc2 lowers fasting blood glucose (FBG) without affecting fasting plasma insulin (FPI) while, in isolated islets, glucose-6-phosphatase activity and glucose cycling are abolished and glucose-stimulated insulin secretion (GSIS) is enhanced at submaximal but not high glucose. These observations are all consistent with a model in which G6PC2 regulates the sensitivity of GSIS to glucose by opposing the action of glucokinase. G6PC2 is highly expressed in human and
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Moonira, Tabassum, Shruti S. Chachra, Brian E. Ford, et al. "Metformin lowers glucose 6-phosphate in hepatocytes by activation of glycolysis downstream of glucose phosphorylation." Journal of Biological Chemistry 295, no. 10 (2020): 3330–46. http://dx.doi.org/10.1074/jbc.ra120.012533.

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The chronic effects of metformin on liver gluconeogenesis involve repression of the G6pc gene, which is regulated by the carbohydrate-response element–binding protein through raised cellular intermediates of glucose metabolism. In this study we determined the candidate mechanisms by which metformin lowers glucose 6-phosphate (G6P) in mouse and rat hepatocytes challenged with high glucose or gluconeogenic precursors. Cell metformin loads in the therapeutic range lowered cell G6P but not ATP and decreased G6pc mRNA at high glucose. The G6P lowering by metformin was mimicked by a complex 1 inhibi
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Nyce, Jonathan W. "Detection of a novel, primate-specific ‘kill switch’ tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53." Endocrine-Related Cancer 25, no. 11 (2018): R497—R517. http://dx.doi.org/10.1530/erc-18-0241.

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The activation of TP53 is well known to exert tumor suppressive effects. We have detected aprimate-specificadrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has beeninactivated. DHEA is anuncompetitiveinhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell. Uncompetitive inhibition is otherwise unknown in natural systems because it becomesirreversiblein the presence of high concentrations of substrate and inhibi
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Salgado, M. C., I. Metón, M. Egea, and I. V. Baanante. "Transcriptional regulation of glucose-6-phosphatase catalytic subunit promoter by insulin and glucose in the carnivorous fish, Sparus aurata." Journal of Molecular Endocrinology 33, no. 3 (2004): 783–95. http://dx.doi.org/10.1677/jme.1.01552.

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Increase in glucose-6-phosphatase catalytic subunit (G6Pase, G6pc) transcription enhances hepatic glucose production in non-insulin-dependent diabetes mellitus (NIDDM). The fact that carnivorous fish is an alternative model to study NIDDM led us to clone and characterise the first G6pc promoter region reported for fish and non-mammalian animals. The 5′-flanking region of G6pc from gilthead sea bream (Sparus aurata) was isolated by chromosome walking. With SMART RACE-PCR, the transcription start site was located 106 base pairs (bp) upstream of the translational start. Transfection analysis in H
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Resaz, Roberta, Davide Cangelosi, Martina Morini, et al. "Circulating exosomal microRNAs as potential biomarkers of hepatic injury and inflammation in a murine model of glycogen storage disease type 1a." Disease Models & Mechanisms 13, no. 9 (2020): dmm043364. http://dx.doi.org/10.1242/dmm.043364.

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ABSTRACTMost patients affected by glycogen storage disease type 1a (GSD1a), an inherited metabolic disorder caused by mutations in the enzyme glucose-6-phosphatase-α (G6Pase-α), develop renal and liver complications, including the development of hepatocellular adenoma/carcinoma. The purpose of this study was to identify potential biomarkers of the pathophysiology of the GSD1a-affected liver. To this end, we used the plasma exosomes of a murine model of GSD1a, the LS-G6pc−/− mouse, to uncover the modulation in microRNA expression associated with the disease. The microRNAs differentially express
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Gautam, Sudeep, Lisa Zhang, Irina Arnaoutova, Cheol Lee, Brian C. Mansfield, and Janice Y. Chou. "The signaling pathways implicated in impairment of hepatic autophagy in glycogen storage disease type Ia." Human Molecular Genetics 29, no. 5 (2020): 834–44. http://dx.doi.org/10.1093/hmg/ddaa007.

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Abstract Glucose-6-phosphatase-α (G6Pase-α or G6PC) deficiency in glycogen storage disease type-Ia (GSD-Ia) leads to impaired hepatic autophagy, a recycling process important for cellular metabolism and homeostasis. Autophagy can be regulated by several energy sensing pathways, including sirtuin 1 (SIRT1), forkhead box O (FoxO), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-α (PPAR-α), and mammalian target of rapamycin (mTOR). Using 10-day old global G6pc-deficient (G6pc−/−) mice, hepatic autophagy impairment was attributed to activation of mTOR and inhibition
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Saeed, Ali, Joanne A. Hoogerland, Hanna Wessel, et al. "Glycogen storage disease type 1a is associated with disturbed vitamin A metabolism and elevated serum retinol levels." Human Molecular Genetics 29, no. 2 (2019): 264–73. http://dx.doi.org/10.1093/hmg/ddz283.

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Abstract Glycogen storage disease type 1a (GSD Ia) is an inborn error of metabolism caused by mutations in the G6PC gene, encoding the catalytic subunit of glucose-6-phosphatase. Early symptoms include severe fasting intolerance, failure to thrive and hepatomegaly, biochemically associated with nonketotic hypoglycemia, fasting hyperlactidemia, hyperuricemia and hyperlipidemia. Dietary management is the cornerstone of treatment aiming at maintaining euglycemia, prevention of secondary metabolic perturbations and long-term complications, including liver (hepatocellular adenomas and carcinomas),
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Dorum, S., and O. Gorukmez. "A novel mutation in a newborn baby leading to glycogen storage disease type Ia." Balkan Journal of Medical Genetics 21, no. 2 (2018): 55–57. http://dx.doi.org/10.2478/bjmg-2018-0018.

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Abstract Glycogen storage disease type Ia (GSD1A) is caused by mutations in the G6PC gene. The G6PC gene was first cloned in 1993. Since then, many different mutations have been identified leading to this disease. Hepatomegaly is one of the important clinical manifestations of the disease. A 23-day-old girl was admitted to the hospital due to respiratory distress. Her physical examination was normal except for tachypnea. She had hypoglycemia, lactic academia, hyperlipidemia and hyperuricemia. With these clinical findings, GSD1A was considered in the patient and the diagnosis was genetically co
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Beaudry, Jean-Bernard, Christophe E. Pierreux, Graham P. Hayhurst та ін. "Threshold Levels of Hepatocyte Nuclear Factor 6 (HNF-6) Acting in Synergy with HNF-4 and PGC-1α Are Required for Time-Specific Gene Expression during Liver Development". Molecular and Cellular Biology 26, № 16 (2006): 6037–46. http://dx.doi.org/10.1128/mcb.02445-05.

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ABSTRACT During liver development, hepatocytes undergo a maturation process that leads to the fully differentiated state. This relies at least in part on the coordinated action of liver-enriched transcription factors (LETFs), but little is known about the dynamics of this coordination. In this context we investigate here the role of the LETF hepatocyte nuclear factor 6 (HNF-6; also called Onecut-1) during hepatocyte differentiation. We show that HNF-6 knockout mouse fetuses have delayed expression of glucose-6-phosphatase (g6pc), which catalyzes the final step of gluconeogenesis and is a late
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Arden, Catherine, Susan J. Tudhope, John L. Petrie, et al. "Fructose 2,6-bisphosphate is essential for glucose-regulated gene transcription of glucose-6-phosphatase and other ChREBP target genes in hepatocytes." Biochemical Journal 443, no. 1 (2012): 111–23. http://dx.doi.org/10.1042/bj20111280.

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Glucose metabolism in the liver activates the transcription of various genes encoding enzymes of glycolysis and lipogenesis and also G6pc (glucose-6-phosphatase). Allosteric mechanisms involving glucose 6-phosphate or xylulose 5-phosphate and covalent modification of ChREBP (carbohydrate-response element-binding protein) have been implicated in this mechanism. However, evidence supporting an essential role for a specific metabolite or pathway in hepatocytes remains equivocal. By using diverse substrates and inhibitors and a kinase-deficient bisphosphatase-active variant of the bifunctional enz
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Dissertations / Theses on the topic "G6PC"

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Carlin, Marcelo Paschoalete. "Determinação de mutações nos genes G6PC e G6PT1 em pacientes com glicogenoses tipo Ia e Ib." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308546.

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Orientadores: Carlos Eduardo Steiner, Carmen Silvia Bertuzzo<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-17T18:18:42Z (GMT). No. of bitstreams: 1 Carlin_MarceloPaschoalete_M.pdf: 1614647 bytes, checksum: 62e5b428719069b2b173ab2baf51970f (MD5) Previous issue date: 2011<br>Resumo: A transformação de glicogênio em glicose acontece através de reações químicas realizadas por enzimas específicas e uma deficiência em uma delas leva ao acúmulo de glicogênio, resultando em distúrbios hereditários conhecidos como
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Silva, Aline David. "A esteato-hepatite não alcoólica acompanha-se de superexpressão de SLC2A2, PCK1 e G6PC o que aumenta o efluxo hepático de glicose." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-06092016-092140/.

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A esteato-hepatite não alcoólica (EHNA) apresenta maior efluxo hepático de glicose e hiperglicemia. Estudamos o papel da hiperglicemia e as alterações do metabolismo da glicose em fígado de camundongos obesos (MSG) com EHNA, tratados com dieta hiperlipídica (DH) ou florizina. No fígado dos MSG, independentemente da DH, observou-se: 1) diagnóstico de EHNA; 2) aumento dos mRNAs Tnfa, Il6 e Rela; 3) aumento dos mRNAs Slc2a2, Pck1, G6pc e suas proteínas GLUT2, PEPCK e G6Pase; 4) redução do mRNA Gck e sua proteína GCK; 5) aumento do glicogênio e efluxo de glicose; 6) resistência insulínica, hiperin
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Plona, Kathleen Lynn. "Exploring molecular pathogenesis to streamline future therapeutics in rare diseases using GSD1a as a model." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1624620295305759.

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Chan, Ting-fai. "An analysis of two naturally occurring G6PD deficient mutants, G6PD Campinus and G6PD Fukaya /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31370172.

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Chan, Ting-fai, and 陳定輝. "An analysis of two naturally: occurring G6PD deficient mutants, G6PD Campinus and G6PD Fukaya." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31370172.

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Huang, Yuxiang, and 黃玉祥. "Insights into the molecular basis of the variants: G6PD mahidol and G6PD plymouth." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243150.

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GUSTOVIC, PHILIPPE. "Deficit en g6pd et medicaments." Nice, 1993. http://www.theses.fr/1993NICE6554.

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Pengelly, Robert Joseph. "Structural and mechanistic studies of specific carbohydrate processing enzymes." Thesis, University of St Andrews, 2017. http://hdl.handle.net/10023/10254.

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Guindo, Aldiouma. "G6PD deficiency and its differential protection against malaria." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536844.

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Foulkes, Nicholas F. "Molecular biology of the human G 6-PD gene." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253009.

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Books on the topic "G6PC"

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Conway, David J. Glucose-6-phosphate dehydrogenase (G6PD) activity as an index of thyroidal stimulation and superoxide metabolism in thyroid cancer. University College Dublin, 1996.

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Kück, Katharina. Der Einfluss kompatibler Substanzen und Kryoprotektoren auf die Enzyme Malatdehydrogenase (MDH) und Glucose-6-phosphat-Dehydrogenase (G6P-DH) aus Acrosiphonia arcta (Chlorophyta) der Arktis und Antarktis =: The effect of compatible solutes and cryoprotectors on the enzymes Malate Dehydrogenase (MDH) and Glucose-6-Phosphate Dehydrogenase (G6P-DH) of Acrosiphonia arcta (Chlorophyta) from Arctica and Antarctica. Alfred-Wegener-Institut für Polar- und Meeresforschung, 1997.

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Anderson, Sonya. Cooking with G6PD Deficiency. Lulu Press, Inc., 2020.

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Traoré, Karim, and Aldiouma Guindo. Déficit en G6PD érythrocytaire et paludisme au Mali: Le déficit en G6PD erythrocytaire protege les enfants Dogon contre le paludisme grave au Mali. Omniscriptum, 2011.

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Jolly, Dominique. Le déficit en G6PD: Une affection génétique fréquente et mal connue. Flammarion, 2000.

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Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Patient management issues. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0010.

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Drug use in liver disease 178Drug dosing in liver disease 180Hepatorenal syndrome (HRS) 183Drugs in renal impairment 184Drugs in pregnancy 190Drugs in breastfeeding 194Drugs and dietary considerations 198Glucose 6-phosphate dehydrogenase (G6PD) deficiency 200Drugs in porphyria 202Terminology used in liver disease is summarized in ...
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Frequencies of hemoglobin variants: Thalassemia, the glucose-6-phosphate dehydrogenase deficiency, G6PD variants, and ovalocytosis in human populations. Oxford University Press, 1985.

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McCann, Shaun R. Red blood cells. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0004.

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Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α‎ thalassaemi
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Book chapters on the topic "G6PC"

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Gupta, Arun. "G6PD Deficiency." In Decision Making Through Problem Based Learning in Hematology. Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-8933-1_9.

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Leung, Anskar Y. H., and Edmond S. K. Ma. "G6PD Deficiency." In Haematology and the Asian Patient. CRC Press, 2024. http://dx.doi.org/10.1201/9781003325413-45.

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Fasth, Anders. "SCN4 (G6PC3 Deficiency)." In Encyclopedia of Medical Immunology. Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_153.

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Fasth, Anders. "SCN4 (G6PC3 Deficiency)." In Encyclopedia of Medical Immunology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_153-1.

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Mehlhorn, Heinz. "Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3914.

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Mehlhorn, Heinz. "Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3914-1.

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Theisler, Charles. "Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency." In Adjuvant Medical Care. CRC Press, 2022. http://dx.doi.org/10.1201/b22898-155.

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Al Muqati, Hessa Hazza. "Caring for Patients with Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency." In Manual of Pediatric Cardiac Care. Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-5683-8_45.

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Yeung, Chap-Yung. "Erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency and neonatal hyperbilirubinaemia." In Child Health in the Tropics. Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5012-2_27.

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Cocco, P. L., S. Dessi, P. Manca, R. Cherchi, M. Pisano, and P. F. Todde. "Case-Control Studies on Cancer Risk in G6PD-Deficient Male Populations." In Chemical Carcinogenesis 2. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3694-9_15.

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Conference papers on the topic "G6PC"

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Jácomo, Rafael Henriques, Miguel de Souza Andrade, Gustavo Barcelos Barra, et al. "Estimativa de portadores e afetados por deficiência de G6PD no Brasil: perspectivas de um estudo de triagem genética neonatal." In Resumos do 56º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial. Zeppelini Editorial e Comunicação, 2024. https://doi.org/10.5327/1516-3180.142s1.12559.

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Objetivo: Este estudo investiga as variantes genéticas no gene G6PD no Brasil, focando na análise de sua distribuição entre homens e mulheres utilizando dados laboratoriais. O objetivo principal é estimar a frequência de indivíduos afetados e portadores de variantes associadas à deficiência de G6PD na população brasileira. Método: Conduzido de janeiro de 2019 a janeiro de 2024, este estudo retrospectivo envolveu a análise de dados de um banco de dados laboratorial, todos anonimizados conforme a Lei Geral de Proteção de Dados (LGPD). Incluiu-se uma amostra de indivíduos submetidos à triagem gen
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Camilo, Tiara Lange Felipe Oliveira, Renan Rodrigo Corrêa Gomes, Lorena Karla Da Silva, and Rafaela Vieira De Souza. "A IMPORTÂNCIA DA TRIAGEM PARA DETECÇÃO DA DEFICIENCIA DE GLICOSE-6-FOSFATO-DESIDROGENASE EM ÁREAS ENDÊMICAS DE MALÁRIA NO BRASIL." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/142.

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INTRODUÇÃO: A deficiência de glicose-6-fosfato-desidrogenase (G6PD) enzima citoplasmática dos eritrócitos, responsável pela proteção das hemácias contra ações oxidantes, é uma anormalidade predominante na população negra, tendo padrão de herança recessivo ligado ao cromossomo X, acometendo homens hemizigóticos, podendo ocorrer também em mulheres homozigóticas. É geralmente assintomática, podendo ser desencadeada por fatores que levam ao estresse oxidante, como os antimaláricos. OBJETIVOS: Elencar a importância da realização prévia de exames que possam indicar a deficiência de g6pd em pacientes
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Costa, Juliana Ferreira. "A DEFICIÊNCIA DE G6PD NA ANEMIA HEMOLÍTICA." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/38.

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Introdução: O tempo de circulação de um Eritrócito, em média, corresponde a 120 dias e sua destruição fisiológica ocorre a partir de sua remoção extravascular mediada por macrófagos. Em situações patológicas, a sua retirada da circulação acontece na via intravascular, dando origem às anemias hemolíticas. Dentre as diversas causas para seu desenvolvimento, está a deficiência de Glicose-6-Fosfato-Desidrogenase ou G6PD. Trata-se de uma condição genética associada ao cromossomo X com manifestação sintomática nos homens. Já as mulheres são consideradas portadoras assintomáticas. Objetivos: Compreen
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Silva, Lorena Késsia de Figueiredo, Mariane dos Santos Duarte Spinelli, Euglenia Elbe de Souza Braga Meireles, et al. "Prevalência da deficiência de glicose-6-fosfato desidrogenase e avaliação do sexo predominante em pacientes atendidos em Natal, Rio Grande do Norte." In Resumos do 56º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial. Zeppelini Editorial e Comunicação, 2024. https://doi.org/10.5327/1516-3180.142s1.10193.

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Objetivo: Avaliar a prevalência da deficiência de glicose-6-fosfato desidrogenase (G6PD) em pacientes atendidos em uma unidade de referência. Método: Foram analisadas 86 amostras de sangue de pacientes colhidas com EDTA de ambos os sexos e diversas idades, no período de 1º de janeiro de 2021 a 30 de maio de 2024, com suspeitas clínicas diversas como: anemia a esclarecer, icterícia neonatal e avaliação preventiva para o uso de dapsona, utilizando o método qualitativo (Brewer) associado ao método semiquantitativo (Brewer modificado) para o teste de deficiência de G6PD, doença genética ligada ao
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Khatib, Salem Suhail El. "DEFICIÊNCIA DE G6PD-DOENÇA PREVALENTE E POUCO DIVULGADA." In IV Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2024. http://dx.doi.org/10.51161/hematoclil2024/30281.

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Santiago, Bruno Vitor Martins, Pedro Ernandes Bergamo, Maxuel De Freitas Da Silva, Nicole Faraje Aragão Gonçalves, and Nivaldo Ribeiro Villela. "ANESTESIA PARA ESTUDO ELETROFISIOLÓGICO EM PACIENTE PORTADOR DE DEFICIÊNCIA DE GLICOSE-6-FOSFATO-DESIDROGENASE E METAHEMOGLOBINEMIA – RELATO DE CASO." In II Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbraqui/10.

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Introdução: A deficiência de glicose-6-fosfato desidrogenase (G6PD) e a methemoglobinemia (MetHba) são condições associadas ao desequilíbrio nas reações de redução e oxidação, as quais tornam o ato anestésico desafiador. Objetivo: Relatar um caso de uma anestesia em paciente portador de deficiência de G6PD e MetHba, candidato a estudo eletrofisiológico devido à síndrome de pré-excitação. Relato de caso: Masculino, 20 anos, portador de deficiência de G6PD e MetHba, em uso de propafenona e ácido ascórbico (este último para a MetHba), com proposta de estudo eletrofisiológico. Foi realizada a moni
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Ahmad, Nermen R., Sayran S. Saleh, and Nihad I. Taha. "Biochemical study for glucose -6-phosphate dehydrogenase (G6PD) in Thalassemia patients." In 2ND INTERNATIONAL CONFERENCE ON APPLIED RESEARCH AND ENGINEERING (ICARAE2022). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0170649.

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Tatiane Monteiro Bezerra, Maria, and ANA PAULA DE ANDRADE SILVA. "Anemia hemolítica por deficiência da enzima glicose-6-fosfato desidrogenase (G6PD)." In Simpósio FBJ 2019. Even3, 2020. http://dx.doi.org/10.29327/simpfbj2019.226606.

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Ribeiro, Luiza Matos, Rodrigo Prudêncio Tedeschi, and Livia Maria Della Porta Cosac. "O Polimorfismo da Enzima Glicose-6-Fosfatase Desidrogenase (G6PD) no Carcinoma Hepatocelular." In IV SEVEN INTERNATIONAL MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/sevenivmulti2023-017.

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A glicose-6-fosfatase desidrogenase é uma enzima de importante papel bioquímico. Cuja deficiência pode estar relacionada a supressão do crescimento celular, metástase e geração de tumor. Oferecendo expectativa de proteção para o desenvolvimento de alguns carcinomas, como o hepatocelular (CHC), foco desse estudo. Trata-se de uma revisão bibliográfica, de artigos buscados em plataformas digitais e literatura consolidada. Revisando a fisiopatologia do desenvolvimento de CHC, buscando entender como a G6PD e sua deficiência poderiam estar relacionada.
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Saini, Arun, P. H. Sai, Ishani Gupta, and Dharitri Rath. "ELECTROCHEMICAL-BASED POINT-OF-CARE DETECTION OF G6PD THROUGH BI-SUBSTRATE REACTION." In The 28th International Conference on Miniaturized Systems for Chemistry and Life Sciences - Micro-Total Analysis Systems. Chemical and Biological Microsystems Society, 2024. https://doi.org/10.70477/qmzj4890.

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Reports on the topic "G6PC"

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ชีพสุนทร, พูลลาภ, та ชาลิสา หลุยเจริญ ชีพสุนทร. ผลของการลดระดับการแสดงออกของยีน G6PD ต่อพยาธิกำเนิดในระดับโมเลกุลของเซลล์มะเร็งปอด : รายงานการวิจัย. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2018. https://doi.org/10.58837/chula.res.2018.42.

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ลักษณะสำคัญอย่างหนึ่งของเซลล์มะเร็ง คือ การเปลี่ยนแปลงรูปแบบการใช้พลังงานและเมตาบอลิซึม ซึ่งวิถีเพนโตสฟอสเฟตเป็นวิถีที่ช่วยส่งเสริมการเจริญเติบโตของเซลล์ โดยมีเอนไซม์กลูโคส 6 ฟอสเฟตดีไฮโดรจีเนส (G6PD) เป็นกุญแจสำคัญในปฏิกิริยา จากการศึกษาก่อนหน้าพบว่า G6PD มีการแสดงออกมากขึ้นในเซลล์มะเร็งหลายชนิด เช่น เซลล์มะเร็งตับ อีกทั้งจากการทดสอบระดับการแสดงออกของยีนเทียบกับเซลล์ปกติโดยใช้โปรแกรม CU-DREAM (Connection Up- and Down-Regulation Expression Analysis of Microarrays) พบว่า G6PD มีการแสดงออกเพิ่มมากขึ้นในเซลล์มะเร็งตับ และปอด โดยมะเร็งปอดสามารถพบได้เป็นอันดับ 2 ของผู้ป่วยมะเร็ง อีกทั้งอัตราการรอดช
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หลุยเจริญ ชีพสุนทร, ชาลิสา, та พูลลาภ ชีพสุนทร. ผลของภาวะพร่องเอนไซม์ G6PD ต่อการเสื่อมของเซลล์ไตในโรคเบาหวาน. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2018. https://doi.org/10.58837/chula.res.2018.30.

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เอนไซม์ glucose 6-phosphate dehydrogenase (G6PD) เป็นเอนไซม์ที่พบได้ในทุกเซลล์ของร่างกาย มีหน้าที่สร้าง nicotinamide adenine dinucleotide (NADPH) จากวิถี pentose phosphate pathway (PPP) เพื่อช่วยป้องกันภาวะ oxidative stress ภายในเซลล์ด้วยการรักษาระดับ reduced glutathione (GSH) ความผิดปกติที่เกิดขึ้นกับเอนไซม์ G6PD ส่งผลกระทบต่อเซลล์จากภาวะ oxidative stress เช่น ภาวะพร่องเอนไซม์ G6PD สามารถเหนี่ยวนำให้เซลล์ไตเกิด apoptosis และ nephropathy นอกจากนี้ยังพบภาวะพร่องเอนไซม์ G6PD เพิ่มสูงขึ้นในผู้ป่วยเบาหวานเมื่อเทียบกับคนปกติ ด้วยเหตุนี้จึงเป็นที่มาของการศึกษาวิจัยบทบาทของภาวะพร่องเอนไซม์ G6PD ในเซล
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