Literatura académica sobre el tema "GTP Homeostasis"
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Artículos de revistas sobre el tema "GTP Homeostasis"
Shen, Chwan-Li, Jannette M. Dufour, Jonathan M. Miranda, Gurvinder Kaur, Eunhee Chung, Latha Ramalingam, Naima Moustaid-Moussa y Jay J. Cao. "Effect of Dietary Geranylgeraniol and Green Tea Polyphenols on Glucose Homeostasis, Bone Turnover Biomarkers, and Bone Microstructure in Obese Mice". International Journal of Molecular Sciences 24, n.º 2 (4 de enero de 2023): 979. http://dx.doi.org/10.3390/ijms24020979.
Texto completoSeccia, Roberta, Silvia De Santis, Maria A. Di Noia, Ferdinando Palmieri, Daniela V. Miniero, Raffaele Marmo, Eleonora Paradies et al. "Citrate Regulates the Saccharomyces cerevisiae Mitochondrial GDP/GTP Carrier (Ggc1p) by Triggering Unidirectional Transport of GTP". Journal of Fungi 8, n.º 8 (29 de julio de 2022): 795. http://dx.doi.org/10.3390/jof8080795.
Texto completoRodríguez-Fdez, Sonia y Xosé R. Bustelo. "Rho GTPases in Skeletal Muscle Development and Homeostasis". Cells 10, n.º 11 (2 de noviembre de 2021): 2984. http://dx.doi.org/10.3390/cells10112984.
Texto completoKhadilkar, Rohan J., Diana Rodrigues, Ridim Dadasaheb Mote, Arghyashree Roychowdhury Sinha, Vani Kulkarni, Srivathsa Subramanya Magadi y Maneesha S. Inamdar. "ARF1–GTP regulates Asrij to provide endocytic control ofDrosophilablood cell homeostasis". Proceedings of the National Academy of Sciences 111, n.º 13 (18 de marzo de 2014): 4898–903. http://dx.doi.org/10.1073/pnas.1303559111.
Texto completoMazhab-Jafari, Mohammad T., Christopher B. Marshall, Noboru Ishiyama, Jason Ho, Vanessa Di Palma, Vuk Stambolic y Mitsuhiko Ikura. "An Autoinhibited Noncanonical Mechanism of GTP Hydrolysis by Rheb Maintains mTORC1 Homeostasis". Structure 20, n.º 9 (septiembre de 2012): 1528–39. http://dx.doi.org/10.1016/j.str.2012.06.013.
Texto completoChen, Hui-Jie, Na Li, Ye Luo, Yong-Liang Jiang, Cong-Zhao Zhou, Yuxing Chen y Qiong Li. "The GDP-switched GAF domain of DcpA modulates the concerted synthesis/hydrolysis of c-di-GMP in Mycobacterium smegmatis". Biochemical Journal 475, n.º 7 (9 de abril de 2018): 1295–308. http://dx.doi.org/10.1042/bcj20180079.
Texto completoKristensson, Maria Alvarado. "The Game of Tubulins". Cells 10, n.º 4 (28 de marzo de 2021): 745. http://dx.doi.org/10.3390/cells10040745.
Texto completoKotelevets, Larissa y Eric Chastre. "Rac1 Signaling: From Intestinal Homeostasis to Colorectal Cancer Metastasis". Cancers 12, n.º 3 (12 de marzo de 2020): 665. http://dx.doi.org/10.3390/cancers12030665.
Texto completoGumataotao, Natalie, K. P. Wasantha Lankathilaka, Brian Bennett y Richard C. Holz. "The iron-type nitrile hydratase activator protein is a GTPase". Biochemical Journal 474, n.º 2 (6 de enero de 2017): 247–58. http://dx.doi.org/10.1042/bcj20160884.
Texto completoMori, Risa y Takashi Toda. "The dual role of fission yeast Tbc1/cofactor C orchestrates microtubule homeostasis in tubulin folding and acts as a GAP for GTPase Alp41/Arl2". Molecular Biology of the Cell 24, n.º 11 (junio de 2013): 1713–24. http://dx.doi.org/10.1091/mbc.e12-11-0792.
Texto completoTesis sobre el tema "GTP Homeostasis"
Zolle, Lapuente Olga C. "Cyclic GMP and calcium homeostasis in endothelial cells". Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367654.
Texto completoAbrahamsson, Niclas. "On the Impact of Bariatric Surgery on Glucose Homeostasis". Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-276381.
Texto completoLusche, Daniel Felix. "Cyclic GMP in the development of the social amoeba Dictyostelium discoideum regulation of calcium homeostasis by cGMP. /". [S.l. : s.n.], 2004. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11482073.
Texto completoSchmitt, Charlotte. "Implication du transporteur intestinal GLUT2 dans l'absorption des sucres et la fonction entéroendocrine". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066465.
Texto completoThe constantly renewing intestinal epithelium handles various essential functions including nutrient absorption and persistence of a barrier between our internal and external environments. Several transporters mediate sugar absorption in the proximal intestine. Among them, GLUT2, a very efficient glucose, fructose and galactose transporter and receptor, is located at the membranes of enterocytes and enteroendocrine cells. The enteroendocrine L-cells produce GLP-1, a strong activator of glucose-induced insulin secretion. This thesis aimed to further decipher the role of intestinal GLUT2 in sugar absorption and enteroendocrine cell function. To address this question, mice lacking GLUT2 specifically in intestinal epithelial cells have been generated and studied. Intestinal GLUT2 invalidation alters intestinal glucose absorption and delays glucose biodistribution to peripheral tissues. This spatial and temporal sugar absorption delay provokes intestinal dysbiosis, favoring gut microbiota having a protective impact on gut homeostasis. Surprisingly, intestinal GLUT2 deletion leads to a strong loss in enteroendocrine L cell density, with no impact on GLP-1 plasma levels. This study highlights critical roles for GLUT2 in sugar absorption and enteroendocrine cell function management. The use of specific GLUT2 inhibitors could be considered to limit body weight gain and metabolic disorders induced by sugar rich diets
Berbel, Luciane Celeste Lazari. "Influência da variação genotípica Glu354Gln do receptor para o GIP sobre a homeostase glicêmica e a sensibilidade insulínica em indivíduos sadios". Universidade Estadual de Londrina. Centro de Ciências da Saúde. Programa de Pós-Graduação em Ciências da Saúde, 2014. http://www.bibliotecadigital.uel.br/document/?code=vtls000189459.
Texto completoThe potential variability in hormonal physiological response after feeding, related to the elevation of postprandial GIP between individuals, arouse interest to evaluate the influence of polymorphisms in the gene for glucose-dependent insulinotropic polypeptide receptor (GIPR) in glucose homeostasis and in pancreatic beta cell function. Altogether 25 adults (12 women, 13 men) with BMI <30 and without metabolic syndrome related diseases were studied. After diet containing 58g of carbohydrates and 28g of lipids, blood samples at baseline (T0) and every 30 minutes until the T150 were collected for measurement of insulin and glucose. The polymorphic GIPR variant Glu354Gln, rs1800437 (SNP-GIPR) was studied in peripheral blood sample through PCR-RFLP. Glucose homeostasis in fasting and postprandial was assessed by calculating HOMA-IR, HOMA-B, area under the curve (AUC) of insulin and glucose, AUCi/AUCg ratio, insulinogenic index (IGI) at each time relative to baseline and IGI/HOMA-IR ratio. In the postprandial curve, 72% of subjects showed glucose peaks and 64% insulin until the T60, with mean of 107 mg/dl and 42.1 IU/mL, respectively. The SNP-GIPR study revealed presence of C allele (C+) in 7 individuals, with 72% of the genotypes GG, 24% GC and 4%CC. There was a significant difference between C + or the group without C allele (C-) in HOMA-B (100 +/- 26 vs. 160 +/- 89 % respectively; p = 0.04).There was no significant difference in the following parameters: AUCg, AUCi, HOMA-IR, IGI, AUCi/AUCg and IGI/HOMA-IR. However, the IGI was higher in the C+ allele group at all time-points (T30, 189%; T60, 147%; T90, 1066%; T120, 29% and T150, 93%), while a similar trend occurred for the IGI/HOMA-R ratio, except in T150. Furthermore, family history of diabetes was positive in 42.9% of C+ subjects, compared with 22.2% from C- group (p = 0.29). In conclusion, we have studied the fasting and postprandial variation of glucose and insulin, including insulin secretions 1st and 2nd phases of healthy subjects; our sample presented genotype distribution similar to the reported population in the literature. C+ and C- euglycemic subjects had similar parameters of beta cell function and insulin sensitivity. In other way, we found variation in HOMA-B according to the genotype, suggesting a reduction in beta cell function related to GIPR polymorphism, without change in insulin sensitivity. The reduction in HOMA-B in healthy individuals, regardless of family history of diabetes, suggests further study of this SNP-GIPR as a possible early marker for the risk of pancreatic failure associated with type 2 diabetes.
Ayari, Sami. "Implication des récepteurs nucléaires HNF-4α et HNF-4γ dans la fonction entéroendocrine et la susceptibilité à l'obésité et au diabète de type II". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066380.
Texto completoObesity and type 2 diabetes (T2D) are metabolic pathologies associated with glucose and energy homeostasis perturbations. Enterohormones are important players in the regulation of the mechanisms disturbed during these pathologies. Among these enterohormones, GLP-1, secreted by enteroendocrine L cells in response to a meal, potentiates insulin secretion by pancreatic β cells and inhibits food intake. The aim of my thesis was to characterize the role of the nuclear receptor HNF-4γ in the energy homeostasis and the endocrine function of the intestine.By using a total and constitutive HNF-4γ knock-out mouse model, our team has highlighted that the loss of hnf-4γ induces an improved glucose tolerance. This effect is due to an increased GLP-1 cell number and GLP-1 plasma levels in response to glucose. All together these data demonstrate for the first time a role of HNF-4γ in glucose homeostasis through a modulation of the enteroendocrine lineage specific for GLP-1 and suggest that its absence could protect mice from the T2D establishment.The loss of HNF-4γ protects mice from body weight gain and glucose intolerance normally induced by six weeks of a high-fat/high-fructose diet demonstrating its involvement in obesity and T2D. HNF-4γ -/- mice are protected from obesity by a greater energy loss in faeces mainly due to lipid malabsorption. These results demonstrate that HNF-4γ is necessary for the intestinal fatty acids uptake.In conclusion, this study highlights the role of the intestinal nuclear receptor HNF-4γ in enteroendocrine function and susceptibility to obesity and T2D
Domingues, Ana Sofia Jesus. "A reporter system to study the role of tRNA modifying enzymes in human proteostasis". Master's thesis, Universidade de Aveiro, 2016. http://hdl.handle.net/10773/21083.
Texto completoA síntese proteica é um processo essencial para que todos os organismos mantenham a homeostasia celular. Os tRNAs são elementos cruciais na síntese proteica, uma vez que codificam a informação genética presente no mRNA. A linha celular HeLa, utilizada neste estudo, foi primeiramente isolada de uma mulher com cancro do colo do útero e desde então tem sido bastante usada na investigação, sendo muito importante no estudo das bases moleculares de muitas doenças. De modo a monitorizar a agregação proteica nesta linha celular, um sistema repórter foi desenvolvido utilizando uma fusão entre HspB1 (Hsp27) e a GFP. HspB1 é um chaperone molecular com capacidade de recrutar outros chaperones e restabelecer a conformação ideal das proteínas em situações de stress. A GFP é uma proteína fluorescente que marca certas condições biológicas de interesse. Para perceber o impacto dos erros da tradução na agregação de proteínas e no surgimento das doenças, o principal objetivo deste estudo foi desenvolver uma linha celular estável (HeLa) expressando um sistema repórter HspB1-GFP, de modo a monitorizar os erros no enovelamento das proteínas em resposta ao stress proteotóxico. Ao longo deste estudo o sistema repórter expressando HspB1-GFP foi desenvolvido com sucesso, permitindo assim a sua utilização para identificar situações fisiológicas e patológicas em que a agregação de proteínas ocorre em células de mamífero.
Protein synthesis is essential for all organisms to maintain cell homeostasis. tRNAs are crucial elements in protein synthesis as they decode the genetic information organized in the mRNA codons. A HeLa cell line, used in this study, was first isolated from a woman with cervical cancer and since then was highly used in biological studies, being extremely important in the study of the molecular basis of several diseases. In order to monitor protein aggregation in this cell line, a reporter system was developed using an HspB1 (Hsp27) and a GFP fusion. HspB1 is a small heat shock protein that, in stress situations, recruits other proteins in order to restore the conformation of the proteins. GFP is a biosensor that reports several cellular conditions of interest. To understand the impact of translation errors on protein aggregation and on the disease arising, the main goal of this study was to develop a stable cell line (HeLa) expressing a reporter system HspB1-GFP to monitor the protein misfolding in response to proteotoxic stress. During this study, the reporter system expressing HspB1-GFP was developed successfully, allowing the identification of physiological and pathological situations where protein aggregation occurs in mammalian cells.
Gupta, Kuldeepkumar Ramnaresh. "(p)ppGpp and c-di-GMP : A Tale of Two Second Messengers in Mycobacterium smegmatis". Thesis, 2015. http://etd.iisc.ac.in/handle/2005/4117.
Texto completoMaida, Adriano. "Effects of Enteroendocrine Hormones on Beta-cell Function and Glucose Homeostasis". Thesis, 2011. http://hdl.handle.net/1807/29800.
Texto completoChiang, Yu-ting. "The Role of p21-activated Protein Kinase 1 in Metabolic Homeostasis". Thesis, 2014. http://hdl.handle.net/1807/44107.
Texto completoLibros sobre el tema "GTP Homeostasis"
Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski y Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.
Texto completoChakera, Aron, William G. Herrington y Christopher A. O’Callaghan. Disorders of plasma potassium. Editado por Patrick Davey y David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0173.
Texto completoNestler, Eric J. The Biological Basis of Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0001.
Texto completoJoynt, Gavin M. y Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.
Texto completoCapítulos de libros sobre el tema "GTP Homeostasis"
Ransom, Bruce R. "Do Glial Gap Junctions Play a Role in Extracellular Ion Homeostasis?" En Neuroscience Intelligence Unit, 159–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-21935-5_9.
Texto completoNadkarni, Prashant, Oleg G. Chepurny y George G. Holz. "Regulation of Glucose Homeostasis by GLP-1". En Progress in Molecular Biology and Translational Science, 23–65. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-800101-1.00002-8.
Texto completoIorio, Jessica, Lisa Lastraioli y Elena Lastraioli. "Potassium in Solid Cancers". En Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101108.
Texto completoVentura, Raúl y María Isabel Hernández-Alvarez. "Endoplasmic Reticulum: A Hub in Lipid Homeostasis". En Updates on Endoplasmic Reticulum [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105450.
Texto completoRocha-Ortiz, Luis Roberto, Elva Leticia Perez-Luque y Juan Manuel Malacara. "Analysis of Beta-Cell Function and GLP-1 Levels in Carriers of Rs7903146 and Rs12255372TCF7L2Genotypes in Mexican Pre-Diabetic Subjects". En BASIC/TRANSLATIONAL - Diabetes & Glucose Homeostasis: Genetic & Translational Approaches, P2–513—P2–513. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p6.p2-513.
Texto completoPonce, Arturo, Liora Shoshani, Alejandro Ogazon del Toro y Marcelino Cereijido. "Influence of Cardiac Glycosides and Prostaglandins on the Physiology of Epithelial Cells". En Human Physiology - Annual Volume 2023 [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.111845.
Texto completoPearce, Simon H. S. y Catherine J. Owen. "Endocrine Autoimmunity". En Oxford Textbook of Endocrinology and Diabetes 3e, editado por John A. H. Wass, Wiebke Arlt y Robert K. Semple, 50–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0007.
Texto completoNasir, Aimen, Irum Shahzadi y Ismat Nawaz. "Molecular Mechanisms and Strategies Contributing toward Abiotic Stress Tolerance in Plants". En Abiotic Stress in Plants - Adaptations to Climate Change [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109838.
Texto completoJežek, Petr, Blanka Holendová, Martin Jabůrek, Jan Tauber, Andrea Dlasková y Lydie Plecitá-Hlavatá. "Redox Signaling is Essential for Insulin Secretion". En Type 2 Diabetes [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94312.
Texto completoInformes sobre el tema "GTP Homeostasis"
Splitter, Gary A., Menachem Banai y Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, enero de 2011. http://dx.doi.org/10.32747/2011.7699864.bard.
Texto completoChalutz, Edo, Michael Wisniewski, Samir Droby, Yael Eilam y Ilan Chet. Mode of Action of Yeast Biocontrol Agents of Postharvest Diseases of Fruits. United States Department of Agriculture, junio de 1996. http://dx.doi.org/10.32747/1996.7613025.bard.
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