Bibliografías temáticas / Hexokinase

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Literatura académica sobre el tema "Hexokinase"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 11 de marzo de 2023

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Artículos de revistas sobre el tema "Hexokinase"

1

Radojković, J. y T. Ureta. "Hexokinase isoenzymes from the Novikoff hepatoma. Purification, kinetic and structural characterization, with emphasis on hexokinase C". Biochemical Journal 242, n.º 3 (15 de marzo de 1987): 895–903. http://dx.doi.org/10.1042/bj2420895.

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The purification to homogeneity of hexokinases B and C from the cytosol of rat Novikoff hepatoma was achieved by a protocol using an initial chromatography on Blue 2-agarose to separate the isoenzymes from each other. After that step each hexokinase was subjected to chromatography on DEAE-cellulose, hydroxyapatite and Sephacryl S-300, followed by re-chromatography on hydroxyapatite. The final preparations of hexokinases B and C had specific activities of 86 and 23.5 units/mg of protein respectively, and gave single bands on electrophoresis under non-denaturing conditions or in SDS/polyacrylamide gels. Mr values of about 100,000 were found for both isoenzymes either by Sephacryl S-300 chromatography or by SDS/polyacrylamide-gel electrophoresis. Values of apparent Km for glucose and ATP of pure hexokinase B were similar to those reported for the enzyme from other sources. The apparent Km value for glucose of hexokinase C was 0.025 mM. Marked inhibition of hexokinase C by glucose concentrations above 0.2 mM was found. The effect was partially relieved by ATP concentrations above 1 mM and was independent of pH. Glucose 6-phosphate was inhibitory, but the Ki value (0.18 mM) is higher than those reported for other animal hexokinases. The amino acid composition of hexokinase C was found to be similar to those reported for hexokinases B and D. Also, an immune serum directed against hexokinase A was able, at low dilutions, to bind hexokinases B and C. An immune serum directed against hexokinase C was able, at low dilutions, to bind hexokinase B and also, but weakly, hexokinase A.
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2

Magnani, M., G. Serafini y V. Stocchi. "Hexokinase type I multiplicity in human erythrocytes". Biochemical Journal 254, n.º 2 (1 de septiembre de 1988): 617–20. http://dx.doi.org/10.1042/bj2540617.

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Hexokinase I in human erythrocytes exists in multiple molecular forms that differ in isoelectric points. By means of Western blotting and immunodetection of total glucose-phosphorylating activity by using an antibody raised in rabbit against homogeneous human placenta hexokinase I, a single protein band was detected. Identical results were also obtained by immunoaffinity chromatography of the partially purified enzyme. Separation of the three major hexokinase I subtypes (Ia, Ib and Ic) by h.p.l.c. ion-exchange chromatography and immunodetection following electrophoretic blotting confirmed that each hexokinase subtype showed the same apparent Mr of 112,000, which is the value obtained for the high-Mr hexokinase I from human placenta. Purification of erythrocyte hexokinase by a combination of several procedures including dye-ligand and affinity chromatography that were previously successfully applied to the purification of other mammalian hexokinases type I produced a 35,000-fold-purified enzyme that showed several contaminants after SDS/polyacrylamide-gel electrophoresis. Only one of these peptides was found to be recognized by anti-(hexokinase I) IgG, suggesting that proteolytic degradation does not occur and that hexokinases Ia, Ib and Ic have the same apparent Mr.
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3

Vischer, U., B. Blondel, C. B. Wollheim, W. Höppner, H. J. Seitz y P. B. Iynedjian. "Hexokinase isoenzymes of RIN-m5F insulinoma cells. Expression of glucokinase gene in insulin-producing cells". Biochemical Journal 241, n.º 1 (1 de enero de 1987): 249–55. http://dx.doi.org/10.1042/bj2410249.

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We have analysed the pattern of expression of the hexokinase isoenzyme group in RIN-m5F insulinoma cells. Three hexokinase forms were resolved by DEAE-cellulose chromatography. The most abundant isoenzyme co-eluted with hexokinase type II from rat adipose tissue and displayed a Km for glucose of 0.15 mM, similar to the adipose-tissue enzyme. Hexokinase type II was in large part associated with a particulate subcellular fraction in RIN-m5F cells. The two other hexokinases separated by ion-exchange chromatography were an enzyme similar to hexokinase type I from brain and glucokinase (or hexokinase type IV). The latter isoenzyme was identified as the liver-type glucokinase by the following properties: co-elution with hepatic glucokinase from DEAE-cellulose and DEAE-Sephadex; sigmoid saturation kinetics with glucose with half-maximal velocity at 5.6 mM and Hill coefficient (h) of 1.54; suppression of enzyme activity by antibodies raised against rat liver glucokinase; apparent Mr of 56,500 and pI of 5.6, as shown by immunoblotting after one- and two-dimensional gel electrophoresis; peptide map identical with that of hepatic glucokinase after proteolysis with chymotrypsin and papain. These data indicate that the gene coding for hepatic glucokinase is expressed in RIN-m5F cells, a finding consistent with indirect evidence for the presence of glucokinase in the beta-cell of the islet of Langerhans. On the other hand, the overall pattern of hexokinases is distinctly different in RIN-m5F cells and islets of Langerhans, since hexokinase type II appears to be lacking in islets. Alteration in hexokinase expression after tumoral transformation has been reported in other systems.
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van Wijk, Richard, Gert Rijksen, Eric G. Huizinga, Hendrik K. Nieuwenhuis y Wouter W. van Solinge. "HK Utrecht: missense mutation in the active site of human hexokinase associated with hexokinase deficiency and severe nonspherocytic hemolytic anemia". Blood 101, n.º 1 (1 de enero de 2003): 345–47. http://dx.doi.org/10.1182/blood-2002-06-1851.

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Abstract Hexokinase deficiency is a rare autosomal recessive disease with a clinical phenotype of severe hemolysis. We report a novel homozygous missense mutation in exon 15 (c.2039C>G, HK [hexokinase] Utrecht) of HK1, the gene that encodes red blood cell–specific hexokinase-R, in a patient previously diagnosed with hexokinase deficiency. The Thr680Ser substitution predicted by this mutation affects a highly conserved residue in the enzyme's active site that interacts with phosphate moieties of adenosine diphosphate, adenosine triphosphate (ATP), and inhibitor glucose-6-phosphate. We correlated the molecular data to the severe clinical phenotype of the patient by means of altered enzymatic properties of partially purified hexokinase from the patient, notably with respect to Mg2+-ATP binding. These kinetic properties contradict those obtained from a recombinant mutant brain hexokinase-I with the same Thr680Ser substitution. This contradiction thereby stresses the valuable contribution of studying patients with hexokinase deficiency to achieve a better understanding of hexokinase's key role in glycolysis.
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Bergmanni, Fritz y Leon Mejnartowicz. "Substrate specificity of glucokinase and fructokinase of several conifer species". Acta Societatis Botanicorum Poloniae 71, n.º 2 (2014): 125–27. http://dx.doi.org/10.5586/asbp.2002.014.

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Annual plant species were found to have several distinct classes of hexokinases which are specific for different hexoses, such as glucose, fructose and mannose. In conifers one isozyme of hexokinase could be found in genetic studies if only glucose was employed as substrate. If fructose was substituted for glucose, another isozyme zone different from the common hexokinase could be observed in zymograms of extracts from seed tissues of Norway spruce, Scots pine and silver fir. Hence these three conifer species possess at least two different hexokinases, glucokinase and fructokinase.
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Galina, A., M. Reis, M. C. Albuquerque, A. G. Puyou, M. T. G. Puyou y L. de Meis. "Different properties of the mitochondrial and cytosolic hexokinases in maize roots". Biochemical Journal 309, n.º 1 (1 de julio de 1995): 105–12. http://dx.doi.org/10.1042/bj3090105.

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After tissue homogenization, 43% of the total hexokinase activity found in maize radicles was recovered in the mitochondrial fraction and 35% was soluble, in the cytosol. The maize submitochondrial particles obtained after mitochondrial sonication retained a high hexokinase activity. The mitochondrial respiration (state 4 rate) was activated by glucose. This activation was blocked by carboxyatractyloside (0.5 mM) and by oligomycin (2 micrograms/ml). The affinities for ATP and glucose of both soluble and membrane-bound maize hexokinases are similar to those of yeast hexokinase. The Km for ATP of these different forms of hexokinase varied between 0.15 and 0.37 mM, and the Km for glucose between 0.05 and 0.13 mM. A major difference between the two maize hexokinase forms is that only the mitochondrial enzyme was strongly inhibited by ADP (Ki 0.04 mM). The soluble forms of hexokinase found both in the cytosol of maize radicles and in yeast are not inhibited by ADP. In a previous report [de Meis, Grieco and Galina (1992) FEBS Lett. 308, 197-201] it was shown that the mitochondrial F1-F0-ATPase can use glucose 6-phosphate and yeast hexokinase as an ATP regenerating system. We now show that the membrane-bound hexokinase and glucose 6-phosphate can also serve as an ATP regenerating system for the mitochondria of maize radicles provided that the ADP concentration is kept below 0.05 mM. Higher ADP concentrations inhibit the reverse reaction of the mitochondrial hexokinase.
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7

Victorovich, Khrustalev Vladislav, Lelevich Sergey Vladimirovich y Barkovsky Eugene Victorovich. "Zebra Finch Glucokinase Containing Two Homologous Halves Is an In Silico Chimera". ISRN Computational Biology 2013 (7 de noviembre de 2013): 1–6. http://dx.doi.org/10.1155/2013/790240.

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Chimerical nature of the gene annotated as Zebra finch (Taeniopygia guttata) glucokinase (hexokinase IV) has been proved in this study. N-half of the protein encoded by that gene shows similarity with glucokinase from other vertebrates, while its C-half shows similarity with C-halves of hexokinases II. We mapped 7 new exons coding for N-half of hexokinase II and 4 new exons coding for glucokinase of Zebra finch. Finally, we reconstructed normal genes coding for Zebra finch glucokinase and hexokinase II which are situated in “head-to-tail” orientation on the chromosome 22. Because of the error in gene annotation, exons encoding N-half of normal glucokinase have been fused with exons encoding C-half of normal hexokinase II, even though they are separated from each other by the sequence 98066 nucleotides in length.
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8

Magnani, M., M. Bianchi, A. Casabianca, V. Stocchi, A. Daniele, F. Altruda, M. Ferrone y L. Silengo. "A recombinant human ‘mini’-hexokinase is catalytically active and regulated by hexose 6-phosphates". Biochemical Journal 285, n.º 1 (1 de julio de 1992): 193–99. http://dx.doi.org/10.1042/bj2850193.

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Mammalian hexokinase type I is a 100 kDa enzyme that has been considered to be evolved from an ancestral 50 kDa yeast-type hexokinase, insensitive to product inhibition, by gene duplication and fusion. According to this model, and based on many experimental data, the catalytic site is associated with the C-terminal half of the enzyme, although an allosteric site for the binding of glucose 6-phosphate could be present on the N-terminal half of the molecule. We have isolated a cDNA clone of hexokinase from a lambda gt11 human placenta library comprising 2658 bp, containing a single open reading frame of 1893 nucleotides, which encodes a truncate form of hexokinase starting from asparagine-287 to the terminal serine-917. This clone was further digested with restriction enzyme NcoI to obtain almost only the C-terminal half of human hexokinase starting from methionine-455 to the terminal amino acid and was overexpressed in active form in Escherichia coli and purified by ion-exchange h.p.l.c. The overexpressed ‘mini’-hexokinase was found not only to catalyse glucose phosphorylation, but also to be inhibited by glucose 6-phosphate and other mono- and bis-phosphate sugars exactly like the complete mammalian enzyme. These results suggest that the C-terminal half of human hexokinase, in addition to the catalytic site, also contains the regulatory site and that the evolutionary relationship between the hexokinases should be reconsidered by including the appearance of a regulatory site before the gene duplication.
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Wasserman, David H. "Insulin, Muscle Glucose Uptake, and Hexokinase: Revisiting the Road Not Taken". Physiology 37, n.º 3 (1 de mayo de 2022): 115–27. http://dx.doi.org/10.1152/physiol.00034.2021.

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Research conducted over the last 50 yr has provided insight into the mechanisms by which insulin stimulates glucose transport across the skeletal muscle cell membrane Transport alone, however, does not result in net glucose uptake as free glucose equilibrates across the cell membrane and is not metabolized. Glucose uptake requires that glucose is phosphorylated by hexokinases. Phosphorylated glucose cannot leave the cell and is the substrate for metabolism. It is indisputable that glucose phosphorylation is essential for glucose uptake. Major advances have been made in defining the regulation of the insulin-stimulated glucose transporter (GLUT4) in skeletal muscle. By contrast, the insulin-regulated hexokinase (hexokinase II) parallels Robert Frost’s “The Road Not Taken.” Here the case is made that an understanding of glucose phosphorylation by hexokinase II is necessary to define the regulation of skeletal muscle glucose uptake in health and insulin resistance. Results of studies from different physiological disciplines that have elegantly described how hexokinase II can be regulated are summarized to provide a framework for potential application to skeletal muscle. Mechanisms by which hexokinase II is regulated in skeletal muscle await rigorous examination.
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Khan, Md Wasim, Xianzhong Ding, Scott J. Cotler, Michael Clarke y Brian T. Layden. "Studies on the Tissue Localization of HKDC1, a Putative Novel Fifth Hexokinase, in Humans". Journal of Histochemistry & Cytochemistry 66, n.º 5 (5 de febrero de 2018): 385–92. http://dx.doi.org/10.1369/0022155418756849.

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Hexokinase domain component 1 (HKDC1) is a recently discovered novel protein, which is being promoted as a putative fifth hexokinase. Although the exact role HKDC1 plays in physiology is still unclear, it has been shown to be important during pregnancy in the regulation of glucose homeostasis. In this study, we have comprehensively studied the expression pattern of HKDC1 in the human body. Using human tissue sample, immunohistochemistry imaging was performed. Our studies indicate that the tissues with highest HKDC1 expression were the brush border epithelium of the intestines, parts of the pancreas, and lung alveolar macrophages. Future directions will be to understand the role of this fifth hexokinase in these tissues, with a focus on its relative function as compared with other endogenously expressed hexokinases.
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Tesis sobre el tema "Hexokinase"

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Houghton, Franchesca Dawn. "Energy metabolism of the early mouse embryo". Thesis, University of York, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337151.

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2

Dedeoglu, Didem. "Purification And Characterization Of Hexokinase Isoenzymes From Rhizopus Oryzae". Master's thesis, METU, 2005. http://etd.lib.metu.edu.tr/upload/3/12608262/index.pdf.

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ABSTRACT PURIFICATION AND CHARACTERIZATION OF HEXOKINASE ISOENZYMES FROM Rhizopus oryzae Dedeoglu, Didem MS., Department of Biotechnology Supervisor: Prof.Dr. Haluk Hamamci Co-supervisor: Dr. Seyda Aç
ar February 2007, 116 pages Glycolysis is the central metabolic pathway for living organisms. Its regulation is important for the yield of the end products which are industrially important. These end products, like lactic acid produced by Rhizopus oryzae, are industrially important. Rhizopus oryzae is a filamentous fungus producing lactic acid and ethanol. The lactic acid yield of R. oryzae is low (&
#61566
70 %) compared to that of lactic acid bacteria (&
#61502
95 %) still it is noteworthy because R. oryzae produces only the L (+) form of lactic acid which can be metabolized in the human body. The yield of an industrial process should be high for the feasibility of the production of a particular product. If a way can be found increase the flux through the glycolysis the yield of lactic acid may increase as well. Keeping this in mind we wanted to focus on the first step of glycolysis, hexokinase of R. oryzae. Hexokinase catalyzes the reaction that converts glucose to glucose-6-phosphate. In this study for the first time the two isoenzymes of hexokinase of R. oryzae were purified and characterized by biochemically and kinetically Hexokinase has two isoenzymes. The purified enzymes (isoenzymes1 &
isoenzymes2) obeyed Michealis-Menten Kinetics. The Km value of purified isoenzyme 1 is 0.16 mM and isoenzyme 2, 0.21 mM at pH 7.70 for glucose. The Km value of isoenzyme1 for fructose was 28.8 mM. Essentially isoenzyme 2 can not utilize fructose. None of the isoenzymes were inhibited by trehalose-6-phophate.The monomer moleculer weight of isoenzymes were estimated SDS PAGE analysis. There were two different values for molecular weight of isoenzmye 1
62.9 and 42.5 kDa and two values for isoenzyme 2
56.2 and 41.6 kDa
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3

Skaff, David Andrew. "Release of human brain hexokinase from the mitochondrial membrane". [Ames, Iowa : Iowa State University], 2006.

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Lyda, Todd Andrew. "Exploring T. brucei hexokinase biology localization and inhibition studies /". Connect to this title online, 2009. http://etd.lib.clemson.edu/documents/1263396314/.

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Gosmain, Yvan. "Régulation de l'expression du gène de l'hexokinase II en réponse à l'insuline". Lyon 1, 2004. http://www.theses.fr/2004LYO10174.

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L'hexokinase II (HK-II) catalyse la réaction de phosphorylation du glucose en glucose-6-phosphate, permettant ainsi son utilisation. Le diabète de type 2 est caractérisé notamment par un défaut dans l'étape d'entrée/phosphorylation du glucose en réponse à l'insuline. HK-II a été préalablement identifié comme un des gènes anormalement régulés dans cette pathologie. J'ai tout d'abord étudié la régulation in vitro de l'expression du gène HK-II en réponse à l'insuline dans un modèle de cellules musculaires humaines. Nous avons montré que la région -369/-270 du promoteur HK-II confère l'effet transcriptionnel de l'insuline et implique le facteur de transcription SREBP-1. Dans une deuxième partie, une étude physiologique a permis de démontrer que SREBP-1, comme dans le foie et le tissu adipeux, représente un des médiateurs de l'effet transcriptionnel de l'insuline dans le muscle et confirme l'implication de ce facteur dans le contrôle de l'expression de gènes clés du métabolisme des glucides
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Henri, Raphaël. "Mise en place d'une approche de fluxomique chez le fruit de tomate : étude de transformants surexprimant des hexokinases". Bordeaux 2, 2008. http://www.theses.fr/2008BOR21589.

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Chez le fruit de tomate, les teneurs en sucres, acides aminés et acides organiques contribuent à ses caractéristiques gustatives et nutritionnelles et la richesse en protéines et en paroi végétale conditionne en partie sa texture. La connaissance et la compréhension de lka régulation du métabolisme du fruit de tomate sont essentielles pour en améliorer la qualité. Pour cela, pendant cette thèse, nous avons développé un outil de fluxomique, afin de quantifier des flux de carbone dans le métabolisme intermédiaire du péricarpe de fruit de tomate. Nous avons défini des conditions pour l'analyse des flux chez la tomate : des lamelles de péricarpe sont excisées et incubées dans une solution nutritive. La détermination d'une vingtaine de flux a été réalisée sur la variété Ailsa Craig, par marquage des métabolites avec du [1-13C]- et du [2-13C]-glucose dans des conditions d'état stationnaire isotopique et métabolique, après mesure d'enrichissements de composés par RMN du 1H et du 13C et optimisation du calcul des flux du réseau impliqué. Cette étude réalisée sur trois milieux de culture, le milieu MS/10 de référence, le milieu MS dix fois plus concentré, et le milieu MS*+Glutamine à la fois source de carbone et d'azote organique, a permis de tester la robustesse du réseau métabolique. L'application de cette méthodologie à des tomates surexprimant des hexokinases de levure (Y32) et d'Arabidopsis (HK4 et HK37) a permis de définir des perturbations du métabolisme sur HK4 : cette lignée présente une augmentation du cycle des hexoses-P et une réduction du flux de la voie des pentoses phosphates, ce qui pourrait expliquer une réduction de croissance observée in planta
In tomato, concentrations in sugars, amino acids and organic acides determine partly fruit's taste and nutritional characteristics. Moreover, proteins and cell wall determine mainly its texture. Metabolism knowledge and apprehension of its regulation in tomato fruit are essentials to ameliorate its quality. In this work, we have developed a fluxomic tool to quantify carbon fluxes in intermediary metabolism in tomato fruit pericarp. We have first defined conditions for flux analysis in tomato fruit : pericarp slices are excised and incubated in nutritive solution. Determination of about 20 fluxes were performed with Ailsa Craig, using labeling carbon experiments with [1-13C]- and [2-13C]-glucose. After metabolic and isotopic steady state, measurements of metabolite enrichments by 1H and 13C NMR were used to calculate fluxes of the metabolic network. This study, performed on three media, MS/10, the medium reference, MS ten more concentrated and MS*+Glutamine for carbon and organic source, allowed to test the network robustness. Fluxes analyses were then performed on tomato fruits over expressing yeast (Y32) and Arabidopsis hexokinase (HK4 and HK37). We showed metabolism perturbations in HK4 : the increase in the hexoses-P cycle and the decrease in the pentoses-P pathway. These modifications could explain the reduction of fruit development in this genetically affected plant
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Giese, Jens-Otto. "Molekulare und biochemische Charakterisierung der Hexokinase-Genfamilie von Nicotiana tabacum". [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=979533104.

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Karve, Abhijit Avinash. "Functional characterization of hexokinase-like 1(HKL1) from Arabidopsis thaliana". Connect to this title online, 2008. http://etd.lib.clemson.edu/documents/1252423728/.

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Xypnitou, Andromachi. "Biophysical, biochemical and inhibition studies of hexokinases". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/31486.

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Hexokinase is the first enzyme in glycolysis, a major pathway for the generation of energy in all eukaryotes. Mammalian cells have four isoforms (I, II, III, IV) that have different tissue distribution and kinetic properties. Among all isoforms, human hexokinase II (hHKII) has been found to be implicated in many cancers with an increased expression which serves a dual role. First, it maintains the high glycolytic rate of malignant cells (Warburg effect) and second it prevents apoptosis when is bound to mitochondria. Trypanosoma brucei is a parasite that causes Human African Trypanosomiasis (HAT) and has two isoforms with extensive sequence similarity (98%), TbHKI (active form) and TbHK2 (inactive form). The bloodstream-form parasites (BSF) depend exclusively on glycolysis for their survival. The enzyme from both organisms is a validated target for drug-discovery against both cancer and HAT. The aim of the present study is the discovery of novel and specific inhibitors of the enzymes based on their structure. Structure-based drug discovery is commonly used in pharmaceutical companies to aid in the discovery of potent lead compounds. In silico studies were performed in this project using the known crystal structure of human hexokinase I and a model of TbHKI generated by the protein modelling tool Phyre2. The docking programs, AutoDock (AD) and AutoDock Vina (Vina), were chosen to perform the docking of ~3 million compounds to the target molecules and scoring functions calculated the predicted binding affinities of each compound. In total, 28 compounds were purchased to test on the target molecules. In the experimental part of the project, the two enzymes were cloned, expressed and purified. hHKII was successfully purified giving a high yield of active and pure protein. The protein was characterised using many biophysical methods to establish the oligomeric state, the homogeneity and the secondary structure. Crystallisation trials failed and for this reason, N and C domains of the hHKII were purified separately. Unfortunately, the domains also failed to crystallise thus SAXS data were collected and analysed to gain information of their shape at low resolution. A novel inhibition assay was developed and used to identify four weak inhibitors against full length hHKII. TbHKI was difficult to express in a soluble form as most of the protein was expressed in inclusion bodies. The purification resulted in a small amount of active protein that was used entirely for biochemical assays. Four compounds were purchased from the docking of the TbHKI model and one was found to inhibit the enzyme over 65% at 100 μM. Because the active site of both enzymes (hHKII, TbHKI) is well conserved the compounds from hHKII docking were also screened against the TbHKI. Four compounds were found to inhibit this enzyme while one of them was also an inhibitor for human isoform. The remaining three were specific for inhibition of TbHKI.
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Hirsche, Jörg. "Metabole Regulation von Pollenentwicklung und Pollenkeimung durch Zucker". kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2965/.

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Libros sobre el tema "Hexokinase"

1

Bradford, Amanda. Hydration, conformational states and kinetics of yeast hexokinase PII. St. Catharines, Ont: Brock University, Dept. of Biological Sciences, 2002.

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Capítulos de libros sobre el tema "Hexokinase"

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Lackner, K. J. y D. Peetz. "Hexokinase". En Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1441-1.

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Lackner, K. J. y D. Peetz. "Hexokinase". En Springer Reference Medizin, 1109. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1441.

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Schomburg, Dietmar y Dörte Stephan. "Hexokinase". En Enzyme Handbook 13, 555–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59176-1_113.

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Jiang, Shuai. "Hexokinase 2". En Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_7115-1.

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Lackner, K. J. y D. Peetz. "Hexokinase-Methode". En Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1442-1.

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Lackner, K. J. y D. Peetz. "Hexokinase-Methode". En Springer Reference Medizin, 1109–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1442.

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Jiang, Shuai. "Hexokinase 2". En Encyclopedia of Cancer, 2076–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7115.

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Sols, A. "Hexokinase and Glucokinase". En Ciba Foundation Symposium - Control of Glycogen Metabolism, 301–4. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719343.ch21.

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Wilson, J. E. "The Hexokinase Gene Family". En Frontiers in Diabetes, 18–30. Basel: KARGER, 2004. http://dx.doi.org/10.1159/000079004.

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Abrahão-Neto, José, Patricía Infanti y Michele Vitolo. "Hexokinase Production from S. Cerevisiae". En Seventeenth Symposium on Biotechnology for Fuels and Chemicals, 407–12. Totowa, NJ: Humana Press, 1996. http://dx.doi.org/10.1007/978-1-4612-0223-3_37.

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Actas de conferencias sobre el tema "Hexokinase"

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Mahaffety, James P., Caroline R. Amendola, Wei-Ching Chen, Alec Kimmelman, Allan Balmain y Mark R. Philips. "Abstract A13: KRAS4A directly regulates hexokinase 1". En Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-a13.

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JIANG, Yuxin, Michelle KY Siu, Jingjing Wang, Thomas HY Leung, Annie NY Cheung, Hextan YS Ngan y Karen KL Chan. "Abstract LB-270: Hexokinase II (HK2) regulates stemness of ovarian cancer cells". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-270.

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Abela, L., J. Häberle, K. Steindl, S. Vural, L. Dülli, A. Münst, D. Gubler et al. "Severe Dystonic Movement Disorder and Developmental Encephalopathy Due to Hexokinase 1 Mutation". En Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739687.

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Tanbin, Suriyea y Fazia Adyani Ahmad Fuad. "Expression and Purification of Soluble Bacterially-Expressed Human Hexokinase II in E.coli System". En the 2019 9th International Conference. New York, New York, USA: ACM Press, 2019. http://dx.doi.org/10.1145/3326172.3326219.

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Hamm, J., F. Hinrichsen, N. Mishra, K. Shima, N. Sommer, K. Klischies, D. Prasse et al. "Mikrobielle Regulation von Hexokinase 2 koordiniert mitochondrialen Metabolismus und Zelltod bei akuter Colitis". En DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716123.

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Behar, V., R. Yosef, E. Dor-On, N. Amsalem, Y. Horev y OM Becker. "PO-424 modulating hexokinase 2 (HK2) as a novel approach to target metabolic immuno-oncology". En Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.935.

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Ho, Nelson y Brenda L. Coomber. "Abstract 1180: Hexokinase II plays a pivotal role in colorectal cancer cell proliferation and survival". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1180.

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Fang, Yuan, Yizhi Zhan, Yiyi Li, Wei Wang, Dehua Wu y Yi Ding. "Abstract 2914: Hexokinase 2-mediated metabolic reprogramming and apoptosis inhibition supports hepatocellular carcinoma radiation resistance". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2914.

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Fang, Yuan, Yizhi Zhan, Yiyi Li, Wei Wang, Dehua Wu y Yi Ding. "Abstract 2914: Hexokinase 2-mediated metabolic reprogramming and apoptosis inhibition supports hepatocellular carcinoma radiation resistance". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2914.

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Luk, Peter P., Sylvia A. Chung, Han Shen, Stephanie Decollogne, Pierre J. Dilda, Kerrie L. McDonald y Philip J. Hogg. "Abstract 1131: Blocking ATP delivery to hexokinase II in glioblastoma is a promising therapeutic strategy". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1131.

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Informes sobre el tema "Hexokinase"

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Granot, David y Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, enero de 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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Granot, David, Richard Amasino y Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, enero de 2006. http://dx.doi.org/10.32747/2006.7587223.bard.

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Research objectives 1) Analyze the combined effects of hexose phosphorylation and P level in tomato and Arabidopsis plants 2) Analyze the combined effects of hexose phosphorylation and P level in pho1 and pho2 Arabidopsis mutants 3) Clone and analyze the PHO2 gene 4) Select Arabidopsis mutants resistant to high and low P 5) Analyze the Arabidopsis mutants and clone the corresponding genes 6) Survey wild tomato species for growth characteristics at various P levels Background to the topic Hexose phosphorylating enzymes, the first enzymes of sugar metabolism, regulate key processes in plants such as photosynthesis, growth, senescence and vascular transport. We have previously discovered that hexose phosphorylating enzymes might regulate these processes as a function of phosphorous (P) concentration, and might accelerate acquisition of P, one of the most limiting nutrients in the soil. These discoveries have opened new avenues to gain fundamental knowledge about the relationship between P, sugar phosphorylation and plant development. Since both hexose phosphorylating enzymes and P levels affect plant development, their interaction is of major importance for agriculture. Due to the acceleration of senescence caused by the combined effects of hexose phosphorylation and P concentration, traits affecting P uptake may have been lost in the course of cultivation in which fertilization with relatively high P (30 mg/L) are commonly used. We therefore intended to survey wild tomato species for high P-acquisition at low P soil levels. Genetic resources with high P-acquisition will serve not only to generate a segregating population to map the trait and clone the gene, but will also provide a means to follow the trait in classical breeding programs. This approach could potentially be applicable for other crops as well. Major conclusions, solutions, achievements Our results confirm the mutual effect of hexose phosphorylating enzymes and P level on plant development. Two major aspects of this mutual effect arose. One is related to P toxicity in which HXK seems to play a major role, and the second is related to the effect of HXK on P concentration in the plant. Using tomato plants we demonstrated that high HXK activity increased leaf P concentration, and induced P toxicity when leaf P concentration increases above a certain high level. These results further support our prediction that the desired trait of high-P acquisition might have been lost in the course of cultivation and might exist in wild species. Indeed, in a survey of wild species we identified tomato species that acquired P and performed better at low P (in the irrigation water) compared to the cultivated Lycopersicon esculentum species. The connection between hexose phosphorylation and P toxicity has also been shown with the P sensitive species VerticordiaplumosaL . in which P toxicity is manifested by accelerated senescence (Silber et al., 2003). In a previous work we uncovered the phenomenon of sugar induced cell death (SICD) in yeast cells. Subsequently we showed that SICD is dependent on the rate of hexose phosphorylation as determined by Arabidopsis thaliana hexokinase. In this study we have shown that hexokinase dependent SICD has many characteristics of programmed cell death (PCD) (Granot et al., 2003). High hexokinase activity accelerates senescence (a PCD process) of tomato plants, which is further enhanced by high P. Hence, hexokinase mediated PCD might be a general phenomena. Botrytis cinerea is a non-specific, necrotrophic pathogen that attacks many plant species, including tomato. Senescing leaves are particularly susceptible to B. cinerea infection and delaying leaf senescence might reduce this susceptibility. It has been suggested that B. cinerea’s mode of action may be based on induction of precocious senescence. Using tomato plants developed in the course of the preceding BARD grant (IS 2894-97) and characterized throughout this research (Swartzberg et al., 2006), we have shown that B. cinerea indeed induces senescence and is inhibited by autoregulated production of cytokinin (Swartzberg et al., submitted). To further determine how hexokinase mediates sugar effects we have analyzed tomato plants that express Arabidopsis HXK1 (AtHXK1) grown at different P levels in the irrigation water. We found that Arabidopsis hexokinase mediates sugar signalling in tomato plants independently of hexose phosphate (Kandel-Kfir et al., submitted). To study which hexokinase is involved in sugar sensing we searched and identified two additional HXK genes in tomato plants (Kandel-Kfir et al., 2006). Tomato plants have two different hexose phosphorylating enzymes; hexokinases (HXKs) that can phosphorylate either glucose or fructose, and fructokinases (FRKs) that specifically phosphorylate fructose. To complete the search for genes encoding hexose phosphorylating enzymes we identified a forth fructokinase gene (FRK) (German et al., 2004). The intracellular localization of the four tomato HXK and four FRK enzymes has been determined using GFP fusion analysis in tobacco protoplasts (Kandel-Kfir et al., 2006; Hilla-Weissler et al., 2006). One of the HXK isozymes and one of the FRK isozymes are located within plastids. The other three HXK isozymes are associated with the mitochondria while the other three FRK isozymes are dispersed in the cytosol. We concluded that HXK and FRK are spatially separated in plant cytoplasm and accordingly might play different metabolic and perhaps signalling roles. We have started to analyze the role of the various HXK and FRK genes in plant development. So far we found that LeFRK2 is required for xylem development (German et al., 2003). Irrigation with different P levels had no effect on the phenotype of LeFRK2 antisense plants. In the course of this research we developed a rapid method for the analysis of zygosity in transgenic plants (German et al., 2003).
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Granot, David y Sarah M. Assmann. Novel regulation of transpiration by sugar signals within guard cells. United States Department of Agriculture, enero de 2012. http://dx.doi.org/10.32747/2012.7597924.bard.

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Water is the major limiting factor in agriculture and stomata, composed of two guard cells and the pore they circumscribe, are the chief gates controlling plants’ water loss. The prevailing century old paradigm was that sugars act as an osmoticum in guard cells, contributing to the opening of the stomata. In contrast, we discovered that sugars close stomata and the closure is mediated by the sugar-sensing enzyme hexokinase (HXK) that triggers the abscisic acid (ABA)-signaling pathway within the guard cells. This new discovery suggests a sugar-sensing mechanism within guard cells that controls stomatal closure, and supports the existence of a stomatal feedback mechanism that coordinates photosynthesis with transpiration.
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Brosius, III, F. C. Molecular mechanisms of enhanced [18F] fluorodeoxy glucose (FDG) uptake in isochemically injured myocardium: the role of glucose transporter and hexokinase expression. Final technical report for period August 1, 1993--November 30, 1997. Office of Scientific and Technical Information (OSTI), agosto de 1999. http://dx.doi.org/10.2172/763949.

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Bennett, Alan B., Arthur Schaffer y David Granot. Genetic and Biochemical Characterization of Fructose Accumulation: A Strategy to Improve Fruit Quality. United States Department of Agriculture, junio de 2000. http://dx.doi.org/10.32747/2000.7571353.bard.

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The goal of the research project was to evaluate the potential to genetically modify or engineer carbohydrate metabolism in tomato fruit to enhance levels of fructose, a sugar with nearly twice the sweetness value of other sugars. The specific research objectives to achieve that goal were to: 1. Establish the inheritance of a fructose-accumulating trait identified in F1 hybrids of an inferspecific cross between L. hirsutum XL. esculentum and identify linked molecular markers to facilitate its introgression into tomato cultivars. This objective was completed with the genetic data indicating a single major gene, termed Fgr (Fructose glucose ratio), that controlled the partitioning of hexose in the mature fruit. Molecular markers for the gene, were developed to aid introgression of this gene into cultivated tomato. In addition, a second major gene encoding fructokinase 2 (FK2) was found to be a determinant of the fructose to glucose ratio in fruit. The relationship between FK2 and Fgr is epistatic with a combined synergistic effect of the two hirsutum-derived genes on fructose/glucose ratios. 2. Characterize the metabolic and transport properties responsible for high fructose/glucose ratios in fructose-accumulating genotypes. The effect of both the Fgr and FK2 genes on the developmental accumulation of hexoses was studied in a wide range of genetic backgrounds. In all backgrounds the trait is a developmental one and that the increase in fructose to glucose ratio occurs at the breaker stage of fruit development. The following enzymes were assayed, none of which showed differences between genotypes, at either the breaker or ripe stage: invertase, sucrose synthase, FK1, FK2, hexokinase, PGI and PGM. The lack of effect of the FK2 gene on fructokinase activity is surprising and at present we have no explanation for the phenomenon. However, the hirsutum derived Fgr allele was associated with significantly lower levels of phosphorylated glucose, G1c-1-P and G1c-6-P and concomitantly higher levels of the phosphorylated fructose, Fru-6-P, in both the breaker and ripe stage. This suggests a significant role for the isomerase reaction. 3. Develop and implement molecular genetic strategies for the production of transgenic plants with altered levels of enzymes that potentially control fructose/glucose ratios in fruit. This objective focused on manipulating hexokinase and fructokinase expression in transgenic plants. Two highly divergent cDNA clones (Frk1 and Frk2), encoding fructokinase (EC 2.7.1.4), were isolated from tomato (Lycopersicon esculentum) and a potato fructokinase cDNA clone was obtained from Dr. Howard Davies. Following expression in yeast, each fructokinase was identified to code for one of the tomato or potato fructokinase isoforms Transgenic tomato plants were generated with the fructokinase cDNA clone in both sense and antisense orientations and the effect of the gene on tomato plants is currently being studied.
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