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Journal articles on the topic 'Fructose, Aldolase B'

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Published: 4 June 2021

Last updated: 6 February 2022

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1

Cox, Timothy M. "Aldolase B and fructose intolerance." FASEB Journal 8, no. 1 (1994): 62–71. http://dx.doi.org/10.1096/fasebj.8.1.8299892.

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2

SANTAMARIA, Rita, Gabriella ESPOSITO, Luigi VITAGLIANO, et al. "Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase." Biochemical Journal 350, no. 3 (2000): 823–28. http://dx.doi.org/10.1042/bj3500823.

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We have identified a novel hereditary fructose intolerance mutation in the aldolase B gene (i.e. liver aldolase) that causes an arginine-to-glutamine substitution at residue 303 (Arg303 → Gln). We previously described another mutation (Arg303 → Trp) at the same residue. We have expressed the wild-type protein and the two mutated proteins and characterized their kinetic properties. The catalytic efficiency of protein Gln303 is approx. 1/100 that of the wild-type for substrates fructose 1,6-bisphosphate and fructose 1-phosphate. The Trp303 enzyme has a catalytic efficiency approx. 1/4800 that of

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3

AGIUS, Loranne. "Substrate modulation of aldolase B binding in hepatocytes." Biochemical Journal 315, no. 2 (1996): 651–58. http://dx.doi.org/10.1042/bj3150651.

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The binding properties of hepatic aldolase (B) were determined in digitonin-permeabilized rat hepatocytes after the cells had been preincubated with either glycolytic or gluconeogenic substrates. In hepatocytes that had been preincubated in medium containing 5 mM glucose as sole carbohydrate substrate, binding of aldolase to the hepatocyte matrix was maximal at low KCl concentrations (20 mM) or bivalent cation concentrations (1 mM Mg2+) and half-maximal dissociation occurred at 50 mM KCl. Preincubation of hepatocytes (for 10–30 min) with glucose or mannose (10–40 mM), fructose, sorbitol, dihyd

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4

Hopgood, M. F., S. E. Knowles, J. S. Bond, and F. J. Ballard. "Degradation of native and modified forms of fructose-bisphosphate aldolase microinjected into HeLa cells." Biochemical Journal 256, no. 1 (1988): 81–88. http://dx.doi.org/10.1042/bj2560081.

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The uptake and degradation of radiolabelled rabbit muscle fructose-bisphosphate aldolase (EC 4.1.2.13) was studied in HeLa cells microinjected by the erythrocyte ghost fusion system. Labelled aldolase was progressively modified by treatment with GSSG or N-ethylmaleimide (NEM) before microinjection to determine whether these agents, which inactivate and destabilize the enzyme in vitro, affect the half-life of the enzyme in vivo. Increasing exposure of aldolase to GSSG or NEM before microinjection increased the extent of aldolase transfer into the HeLa cells and decreased the proportion of the p

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5

Droppelmann, Cristian A., Doris E. Sáez, Joel L. Asenjo, et al. "A new level of regulation in gluconeogenesis: metabolic state modulates the intracellular localization of aldolase B and its interaction with liver fructose-1,6-bisphosphatase." Biochemical Journal 472, no. 2 (2015): 225–37. http://dx.doi.org/10.1042/bj20150269.

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We have demonstrated that cellular localization of aldolase B and its interaction with fructose-1,6-bisphosphatase-1 (FBPase-1) is modulated by the metabolic conditions. These results show a new level of regulation for aldolase B and FBPase-1 in a cellular context.

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6

RELLOS, Peter, Manir ALI, Michel VIDAILHET, Jurgen SYGUSCH, and Timothy M. COX. "Alteration of substrate specificity by a naturally-occurring aldolase B mutation (Ala337→Val) in fructose intolerance." Biochemical Journal 340, no. 1 (1999): 321–27. http://dx.doi.org/10.1042/bj3400321.

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A molecular analysis of human aldolase B genes in two newborn infants and a 4-year-old child with hereditary fructose intolerance, the offspring of a consanguineous union, has identified the novel mutation Ala337 → Val in homozygous form. This mutation was also detected independently in two other affected individuals who were compound heterozygotes for the prevalent aldolase B allele, Ala149 → Pro, indicating that the mutation causes aldolase B deficiency. To test for the effect of the mutation, catalytically active wild-type human aldolase B and the Val337 variant enzyme were expressed in Esc

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7

Develi-Is, Seval, Gulsev Ozen, Seldag Bekpinar, et al. "Resveratrol improves high-fructose-induced vascular dysfunction in rats." Canadian Journal of Physiology and Pharmacology 92, no. 12 (2014): 1021–27. http://dx.doi.org/10.1139/cjpp-2014-0245.

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High levels of fructose in the diet results in metabolic abnormalities and vascular disorders. In this study, the effect of resveratrol (RES) on vascular relaxation and contraction responses was examined in the aorta of high-fructose (HFr)-fed rats. mRNA expressions of aortic sirtuin 1 (SIRT1), GLUT5, and aldolase B were also investigated. Rats were given fructose (30%) and (or) RES (50 mg·L−1) in their drinking water for 8 weeks. In the HFr-fed rats, plasma levels of arginine and the ratio of arginine:asymmetric dimethylarginine (ADMA) decreased, whereas leptin levels increased. Decreased rel

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8

Simons, Nynke, François-Guillaume Debray, Nicolaas C. Schaper, et al. "Patients With Aldolase B Deficiency Are Characterized by Increased Intrahepatic Triglyceride Content." Journal of Clinical Endocrinology & Metabolism 104, no. 11 (2019): 5056–64. http://dx.doi.org/10.1210/jc.2018-02795.

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Abstract Context There is an ongoing debate about whether and how fructose is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). A recent experimental study showed an increased intrahepatic triglyceride (IHTG) content in mice deficient for aldolase B (aldo B−/−), the enzyme that converts fructose-1-phosphate to triose phosphates. Objective To translate these experimental findings to the human situation. Design Case-control study. Setting Outpatient clinic for inborn errors of metabolism. Patients or Other Participants Patients with hereditary fructose intolerance, a rare

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9

De Souza, M., R. Lindeman, F. Volpato, R. J. Trent, and R. Kamath. "Mutation of aldolase B genes in hereditary fructose intolerance." Lancet 335, no. 8693 (1990): 856. http://dx.doi.org/10.1016/0140-6736(90)90969-c.

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10

BUONO, Pasqualina, Lisa de CONCILIIS, Paola IZZO, and Francesco SALVATORE. "The transcription of the human fructose-bisphosphate aldolase C gene is activated by nerve-growth-factor-induced B factor in human neuroblastoma cells*." Biochemical Journal 323, no. 1 (1997): 245–50. http://dx.doi.org/10.1042/bj3230245.

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A DNA region located at around -200 bp in the 5´ flanking region (region D) of the human brain-type fructose-bisphosphate aldolase (aldolase C) gene has been analysed. We show by transient transfection assay and electrophoretic-mobility-shift assay (EMSA) that the binding of transcriptional activators to region D is much more efficient (80% versus 30%) in human neuroblastoma cells (SKNBE) than in the non-neuronal cell line A1251, which contains low levels of aldolase C mRNA. The sequence of region D, CAAGGTCA, is very similar to the AAAGGTCA motif present in the mouse steroid 21-hydroxylase ge

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11

Cross, N. C. P., T. M. Cox, R. de Franchis, et al. "Molecular analysis of aldolase B genes in hereditary fructose intolerance." Lancet 335, no. 8685 (1990): 306–9. http://dx.doi.org/10.1016/0140-6736(90)90603-3.

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12

Kaiser, Ursula B., and Robert A. Hegele. "Case Report: Heterogeneity of Aldolase B in Hereditary Fructose Intolerance." American Journal of the Medical Sciences 302, no. 6 (1991): 364–68. http://dx.doi.org/10.1097/00000441-199112000-00008.

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13

Sebastio, G., R. de Franchis, P. Strisciuglio, et al. "Aldolase B mutations in Italian families affected by hereditary fructose intolerance." Journal of Medical Genetics 28, no. 4 (1991): 241–43. http://dx.doi.org/10.1136/jmg.28.4.241.

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14

Oppelt, Sarah A., Erin M. Sennott, and Dean R. Tolan. "Aldolase-B knockout in mice phenocopies hereditary fructose intolerance in humans." Molecular Genetics and Metabolism 114, no. 3 (2015): 445–50. http://dx.doi.org/10.1016/j.ymgme.2015.01.001.

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15

Mohammed, Arwa A., Ayman MH ALnaby, Solima M. Sabeel, et al. "Epitope-Based Peptide Vaccine Against Fructose-Bisphosphate Aldolase of Madurella mycetomatis Using Immunoinformatics Approaches." Bioinformatics and Biology Insights 12 (January 2018): 117793221880970. http://dx.doi.org/10.1177/1177932218809703.

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Background: Mycetoma is a distinct body tissue destructive and neglected tropical disease. It is endemic in many tropical and subtropical countries. Mycetoma is caused by bacterial infections ( actinomycetoma) such as Streptomyces somaliensis and Nocardiae or true fungi ( eumycetoma) such as Madurella mycetomatis. To date, treatments fail to cure the infection and the available marketed drugs are expensive and toxic upon prolonged usage. Moreover, no vaccine was prepared yet against mycetoma. Aim: The aim of this study is to predict effective epitope-based vaccine against fructose-bisphosphate

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16

Zhang, Li, Zheng Guo, Jing Huang, Meiruo Liu, Yuandong Wang, and Chaoneng Ji. "Expression, purification, crystallization and preliminary X-ray crystallographic analysis of fructose-1,6-bisphosphate aldolase fromEscherichia coli." Acta Crystallographica Section F Structural Biology Communications 70, no. 10 (2014): 1376–79. http://dx.doi.org/10.1107/s2053230x14018408.

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Fructose-1,6-bisphosphate aldolase is one of the most important enzymes in the glycolytic pathway and catalyzes the reversible cleavage of fructose-1,6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. The full-lengthfbaB gene encoding fructose-1,6-bisphosphate aldolase class I (FBPA I) was cloned fromEscherichia colistrain BL21. FBPA I was overexpressed inE. coliand purified. Biochemical analysis found that the optimum reaction temperature of FBPA I is 330.5 K and that the enzyme has a high temperature tolerance. Crystals of recombinant FBPA I were obtained by the sit

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17

Cao, Wei, Tuanjie Chang, Xiao-qiang Li, Rui Wang та Lingyun Wu. "Dual effects of fructose on ChREBP and FoxO1/3α are responsible for AldoB up-regulation and vascular remodelling". Clinical Science 131, № 4 (2017): 309–25. http://dx.doi.org/10.1042/cs20160251.

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Increased production of methylglyoxal (MG) in vascular tissues is one of the causative factors for vascular remodelling in different subtypes of metabolic syndrome, including hypertension and insulin resistance. Fructose-induced up-regulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms are unclear. Serum levels of MG and fructose were determined in diabetic patients with hypertension. MG level had significant positive correlations with blood pressure and fructose level respectively. C57BL/6 mice were fed with control or fructose-enriched

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18

Benziane, Boubacar, Sylvie Demaretz, Nadia Defontaine, et al. "NKCC2 Surface Expression in Mammalian Cells." Journal of Biological Chemistry 282, no. 46 (2007): 33817–30. http://dx.doi.org/10.1074/jbc.m700195200.

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Apical bumetanide-sensitive Na+-K+-2Cl- co-transporter, termed NKCC2, is the major salt transport pathway in kidney thick ascending limb. NKCC2 surface expression is subject to regulation by intracellular protein trafficking. However, the protein partners involved in the intracellular trafficking of NKCC2 remain unknown. Moreover, studies aimed at under-standing the post-translational regulation of NKCC2 have been hampered by the difficulty to express NKCC2 protein in mammalian cells. Here we were able to express NKCC2 protein in renal epithelial cells by tagging its N-terminal domain. To gain

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19

Stellmacher, Lena, Tatyana Sandalova, Sarah Schneider, Gunter Schneider, Georg A. Sprenger, and Anne K. Samland. "Novel mode of inhibition byD-tagatose 6-phosphate through a Heyns rearrangement in the active site of transaldolase B variants." Acta Crystallographica Section D Structural Biology 72, no. 4 (2016): 467–76. http://dx.doi.org/10.1107/s2059798316001170.

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Transaldolase B (TalB) and D-fructose-6-phosphate aldolase A (FSAA) fromEscherichia coliare C—C bond-forming enzymes. Using kinetic inhibition studies and mass spectrometry, it is shown that enzyme variants of FSAA and TalB that exhibit D-fructose-6-phosphate aldolase activity are inhibited covalently and irreversibly by D-tagatose 6-phosphate (D-T6P), whereas no inhibition was observed for wild-type transaldolase B fromE. coli. The crystal structure of the variant TalBF178Ywith bound sugar phosphate was solved to a resolution of 1.46 Å and revealed a novel mode of covalent inhibition. The sug

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20

Schütz, L. F., K. C. S. Tavares, F. C. Zago, et al. "62 EXPRESSION OF KEY ENZYMES OF THE FRUCTOSE METABOLIC PATHWAY IN NEWBORN IN VITRO-DERIVED CALVES." Reproduction, Fertility and Development 24, no. 1 (2012): 143. http://dx.doi.org/10.1071/rdv24n1ab62.

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Newborn calves derived from IVF often have difficulties in adapting to life ex utero. Among physiological deviations, plasma fructose levels have been shown to be higher in in vitro-produced calves than in controls during the immediate neonatal period. Interestingly, as plasma fructose levels decrease, plasma lactate levels increase in the first hours of life, which may indicate a biochemical relationship between these substrates (Bertolini et al. 2004 Reproduction 128, 341–354). Fructokinase, the primary enzyme in the fructose metabolic pathway, bypasses the regulatory step catalyzed by phosp

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21

Ali, M., G. Tuncman, N. C. Cross, et al. "Null alleles of the aldolase B gene in patients with hereditary fructose intolerance." Journal of Medical Genetics 31, no. 6 (1994): 499–503. http://dx.doi.org/10.1136/jmg.31.6.499.

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22

Esposito, Gabriella, Luigi Vitagliano, Rita Santamaria, Antonietta Viola, Adriana Zagari, and Francesco Salvatore. "Structural and functional analysis of aldolase B mutants related to hereditary fructose intolerance." FEBS Letters 531, no. 2 (2002): 152–56. http://dx.doi.org/10.1016/s0014-5793(02)03451-8.

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23

Gruchota, Jakub, Ewa Pronicka, Lech Korniszewski, et al. "Aldolase B mutations and prevalence of hereditary fructose intolerance in a Polish population." Molecular Genetics and Metabolism 87, no. 4 (2006): 376–78. http://dx.doi.org/10.1016/j.ymgme.2005.11.010.

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24

Brooks, Cydney C., and Dean R. Tolan. "A partially active mutant aldolase B from a patient with hereditary fructose intolerance." FASEB Journal 8, no. 1 (1994): 107–13. http://dx.doi.org/10.1096/fasebj.8.1.8299883.

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25

Bu, Pengcheng, Kai-Yuan Chen, Kun Xiang, et al. "Aldolase B-Mediated Fructose Metabolism Drives Metabolic Reprogramming of Colon Cancer Liver Metastasis." Cell Metabolism 27, no. 6 (2018): 1249–62. http://dx.doi.org/10.1016/j.cmet.2018.04.003.

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26

Morales-Alvarez, Martha Catalina, Maria Laura Ricardo-Silgado, Hernan Nicolas Lemus, Deyanira González-Devia, and Carlos O. Mendivil. "Fructosuria and recurrent hypoglycemia in a patient with a novel c.1693T>A variant in the 3′ untranslated region of the aldolase B gene." SAGE Open Medical Case Reports 7 (January 2019): 2050313X1882309. http://dx.doi.org/10.1177/2050313x18823098.

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Hereditary fructose intolerance, caused by mutations in the ALDOB gene, is an unusual cause of hypoglycemia. ALDOB encodes the enzyme aldolase B, responsible for the hydrolysis of fructose 1-phosphate in the liver. Here, we report the case of a 33-year-old female patient who consulted due to repetitive episodes of weakness, dizziness and headache after food ingestion. An ambulatory 72-h continuous glucose monitoring revealed multiple short hypoglycemic episodes over the day. After biochemical exclusion of other endocrine causes of hypoglycemia, hereditary fructose intolerance seemed a plausibl

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27

Macongonde, Ernesto António, Thais Ceresér Vilela, Giselli Scaini, et al. "Evaluation of theIn VivoandIn VitroEffects of Fructose on Respiratory Chain Complexes in Tissues of Young Rats." Disease Markers 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/312530.

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Hereditary fructose intolerance (HFI) is an autosomal-recessive disorder characterized by fructose and fructose-1-phosphate accumulation in tissues and biological fluids of patients. This disease results from a deficiency of aldolase B, which metabolizes fructose in the liver, kidney, and small intestine. We here investigated the effect of acute fructose administration on the activities of mitochondrial respiratory chain complexes, succinate dehydrogenase (SDH), and malate dehydrogenase (MDH) in cerebral cortex, liver, kidney, and skeletal muscle of male 30-day-old Wistar rats. The rats receiv

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28

Malay, Ali D., Karen N. Allen, and Dean R. Tolan. "Structure of the Thermolabile Mutant Aldolase B, A149P: Molecular Basis of Hereditary Fructose Intolerance." Journal of Molecular Biology 347, no. 1 (2005): 135–44. http://dx.doi.org/10.1016/j.jmb.2005.01.008.

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29

Tolan, Dean R., and Cydney C. Brooks. "Molecular analysis of common aldolase B alleles for hereditary fructose intolerance in North Americans." Biochemical Medicine and Metabolic Biology 48, no. 1 (1992): 19–25. http://dx.doi.org/10.1016/0885-4505(92)90043-x.

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30

Di Dato, Spadarella, Puoti, et al. "Daily Fructose Traces Intake and Liver Injury in Children with Hereditary Fructose Intolerance." Nutrients 11, no. 10 (2019): 2397. http://dx.doi.org/10.3390/nu11102397.

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Background: Hereditary fructose intolerance (HFI) is a rare genetic disorder of fructose metabolism due to aldolase B enzyme deficiency. Treatment consists of fructose, sorbitol, and sucrose (FSS)-free diet. We explore possible correlations between daily fructose traces intake and liver injury biomarkers on a long-term period, in a cohort of young patients affected by HFI. Methods: Patients’ clinical data and fructose daily intake were retrospectively collected. Correlations among fructose intake, serum alanine aminotransferase (ALT) level, carbohydrate-deficient transferrin (CDT) percentage,

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31

Macongonde, Ernesto A., Naithan L. F. Costa, Bruna K. Ferreira, et al. "Neutrotoxic effects of fructose administration in rat brain: implications for fructosemia." Anais da Academia Brasileira de Ciências 87, no. 2 suppl (2015): 1451–59. http://dx.doi.org/10.1590/0001-3765201520140720.

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Fructose accumulates in tissue and body fluids of patients affected by hereditary fructose intolerance (HFI), a disorder caused by the deficiency of aldolase B. We investigated the effect of acute fructose administration on the biochemical profile and on the activities of the Krebs cycle enzymes in the cerebral cortex of young rats. Rats received a subcutaneous injection of NaCl (0.9 %; control group) or fructose solution (5 μmol/g; treated group). Twelve or 24 h after the administration, the animals were euthanized and the cerebral cortices were isolated. Peripheral blood (to obtain the serum

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32

Nickol, Albin A., Norbert E. Müller, Ursula Bausenwein, Manfred G. Bayer, Thomas L. Maier, and Hainfried E. A. Schenk. "Cyanophora paradoxa: Nucleotide Sequence and Phylogeny of the Nucleus Encoded Muroplast Fructose-1,6-bisphosphate Aldolase." Zeitschrift für Naturforschung C 55, no. 11-12 (2000): 991–1003. http://dx.doi.org/10.1515/znc-2000-11-1224.

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Immunoscreening of a C. paradoxa expression library against water soluble muroplast (“cyanelle”) proteins resulted in isolation of a clone encoding the nucleus-encoded muroplast class-II fructose-1,6-bisphosphate aldolase (class-II FBA§). Its nucleotide sequence was determined. The 1432 bp insert, derived from a single-copy gene transcript, bears a reading frame of 1206 bp in length, representing 402 amino acids with 346 amino acids of mature protein. The leading amino acids match structural features necessary for precursor import across chloroplast envelope membranes. In phylogenetic tree top

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33

Elamin Elhasan, Lina Mohamed, Mohamed B. Hassan, Reham M. Elhassan, et al. "Epitope-Based Peptide Vaccine Design against Fructose Bisphosphate Aldolase of Candida glabrata: An Immunoinformatics Approach." Journal of Immunology Research 2021 (May 4, 2021): 1–19. http://dx.doi.org/10.1155/2021/8280925.

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Background. Candida glabrata is a human opportunistic pathogen that can cause life-threatening systemic infections. Although there are multiple effective vaccines against fungal infections and some of these vaccines are engaged in different stages of clinical trials, none of them have yet been approved by the FDA. Aim. Using immunoinformatics approach to predict the most conserved and immunogenic B- and T-cell epitopes from the fructose bisphosphate aldolase (Fba1) protein of C. glabrata. Material and Method. 13 C. glabrata fructose bisphosphate aldolase protein sequences (361 amino acids) wer

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34

Elaković, Ivana, Sanja Kovačević, Danijela Vojnović Milutinović, et al. "Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats." Nutrients 12, no. 11 (2020): 3470. http://dx.doi.org/10.3390/nu12113470.

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The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose overconsumption at a young age induces alterations in glucocorticoid signaling that might contribute to development of metabolic disturbances, we analysed glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1), as well as redox and inflam

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Sanchez-Gutierrez, J. C. "Molecular analysis of the aldolase B gene in patients with hereditary fructose intolerance from Spain." Journal of Medical Genetics 39, no. 9 (2002): 56e—56. http://dx.doi.org/10.1136/jmg.39.9.e56.

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Tolan, Dean R. "Molecular basis of hereditary fructose intolerance: Mutations and polymorphisms in the human aldolase B gene." Human Mutation 6, no. 3 (1995): 210–18. http://dx.doi.org/10.1002/humu.1380060303.

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37

Noro, Mirela, Romina Bertinat, Alejandro Yáñez, Juan Carlos Slebe, and Fernando Wittwer. "Fructose 1,6-bisphosphatase and aldolase B location in organs of sheep supplemented with nonprotein nitrogen." Comparative Clinical Pathology 22, no. 4 (2013): 795–99. http://dx.doi.org/10.1007/s00580-013-1744-2.

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38

Coffee, Erin M., and Dean R. Tolan. "Mutations in the promoter region of the aldolase B gene that cause hereditary fructose intolerance." Journal of Inherited Metabolic Disease 33, no. 6 (2010): 715–25. http://dx.doi.org/10.1007/s10545-010-9192-5.

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39

Elhag, Mustafa, Ruaa Mohamed Alaagib, Nagla Mohamed Ahmed, et al. "Design of Epitope-Based Peptide Vaccine against Pseudomonas aeruginosa Fructose Bisphosphate Aldolase Protein Using Immunoinformatics." Journal of Immunology Research 2020 (November 5, 2020): 1–11. http://dx.doi.org/10.1155/2020/9475058.

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Pseudomonas aeruginosa is a common pathogen that is responsible for serious hospital-acquired infections, ventilator-associated pneumonia, and various sepsis syndromes. Also, it is a multidrug-resistant pathogen recognized for its ubiquity and its intrinsically advanced antibiotic-resistant mechanisms. It usually affects immunocompromised individuals but can also infect immunocompetent individuals. There is no vaccine against it available till now. This study predicts an effective epitope-based vaccine against fructose bisphosphate aldolase (FBA) of Pseudomonas aeruginosa using immunoinformati

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40

Cross, Nicholas C. P., Dean R. Tolan, and Timothy M. Cox. "Catalytic deficiency of human aldolase B in hereditary fructose intolerance caused by a common missense mutation." Cell 53, no. 6 (1988): 881–85. http://dx.doi.org/10.1016/s0092-8674(88)90349-2.

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41

Cross, N. C. P., L. M. Stojanov, and T. M. Cox. "A new aldolase B variant, N334K, is a common cause of hereditary fructose intolerance in Yugoslavia." Nucleic Acids Research 18, no. 7 (1990): 1925. http://dx.doi.org/10.1093/nar/18.7.1925.

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42

Aarskog, NK, and D. Øgreid. "Aldolase B A149P mutation and hereditary fructose intolerance are not associated with sudden infant death syndrome." Acta Paediatrica 84, no. 8 (1995): 947–48. http://dx.doi.org/10.1111/j.1651-2227.1995.tb13801.x.

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43

RELLOS*, Peter, Manir ALI*, Michel VIDAILHET, Jurgen SYGUSCH, and Timothy M. COX. "Alteration of substrate specificity by a naturally-occurring aldolase B mutation (Ala337→Val) in fructose intolerance." Biochemical Journal 340, no. 1 (1999): 321. http://dx.doi.org/10.1042/0264-6021:3400321.

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44

Soderberg, Tim, and Robert C. Alver. "Transaldolase ofMethanocaldococcus jannaschii." Archaea 1, no. 4 (2004): 255–62. http://dx.doi.org/10.1155/2004/608428.

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TheMethanocaldococcus jannaschiigenome contains putative genes for all four nonoxidative pentose phosphate pathway enzymes. Open reading frame (ORF) MJ0960 is a member of themipB/talCfamily of ‘transaldolase-like’ genes, so named because of their similarity to the well-characterized transaldolase B gene family. However, recently, it has been reported that both themipBand thetalCgenes fromEscherichia coliencode novel enzymes with fructose-6-phosphate aldolase activity, not transaldolase activity (Schürmann and Sprenger 2001). The same study reports that other members of themipB/talCfamily appea

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Cho, Eun Jeong, Ashwini K. Devkota, Gabriel Stancu, et al. "A Robust and Cost-Effective Luminescent-Based High-Throughput Assay for Fructose-1,6-Bisphosphate Aldolase A." SLAS DISCOVERY: Advancing the Science of Drug Discovery 25, no. 9 (2020): 1038–46. http://dx.doi.org/10.1177/2472555220926146.

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Hypoxic solid tumors induce the stabilization of hypoxia-inducible factor 1 alpha (HIF1α), which stimulates the expression of many glycolytic enzymes and hypoxia-responsive genes. A high rate of glycolysis supports the energetic and material needs for tumors to grow. Fructose-1,6-bisphosphate aldolase A (ALDOA) is an enzyme in the glycolytic pathway that promotes the expression of HIF1α. Therefore, inhibition of ALDOA activity represents a potential therapeutic approach for a range of cancers by blocking two critical cancer survival mechanisms. Here, we present a luminescence-based strategy to

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Santer, René, Johannes Rischewski, Michaela von Weihe, et al. "The spectrum of aldolase B (ALDOB) mutations and the prevalence of hereditary fructose intolerance in Central Europe." Human Mutation 25, no. 6 (2005): 594. http://dx.doi.org/10.1002/humu.9343.

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Cano, Ainara, Carlos Alcalde, Amaya Belanger-Quintana, et al. "Transferrin Isoforms, Old but New Biomarkers in Hereditary Fructose Intolerance." Journal of Clinical Medicine 10, no. 13 (2021): 2932. http://dx.doi.org/10.3390/jcm10132932.

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Hereditary Fructose Intolerance (HFI) is an autosomal recessive inborn error of metabolism characterised by the deficiency of the hepatic enzyme aldolase B. Its treatment consists in adopting a fructose-, sucrose-, and sorbitol (FSS)-restrictive diet for life. Untreated HFI patients present an abnormal transferrin (Tf) glycosylation pattern due to the inhibition of mannose-6-phosphate isomerase by fructose-1-phosphate. Hence, elevated serum carbohydrate-deficient Tf (CDT) may allow the prompt detection of HFI. The CDT values improve when an FSS-restrictive diet is followed; however, previous d

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Santamaria, R., S. Tamasi, G. Del Piano, et al. "Molecular basis of hereditary fructose intolerance in Italy: identification of two novel mutations in the aldolase B gene." Journal of Medical Genetics 33, no. 9 (1996): 786–88. http://dx.doi.org/10.1136/jmg.33.9.786.

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Hotz, Hansjürg, Thomas Uzzell, and Leszek Berger. "Linkage Groups of Protein-Coding Genes in Western Palearctic Water Frogs Reveal Extensive Evolutionary Conservation." Genetics 147, no. 1 (1997): 255–70. http://dx.doi.org/10.1093/genetics/147.1.255.

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Abstract Among progeny of a hybrid (Rana shqiperica × R. lessonae) × R lessonae, 14 of 22 loci form four linkage groups (LGs): (1) mitochondrial aspartate aminotransferase, carbonate dehydratase-2, esterase 4, peptidase D; (2) mannosephosphate isomerase, lactate dehydrogenase-B, sex, hexokinase-1, peptidase B; (3) albumin, fructose-biphosphatase-1, guanine deaminase; (4) mitochondrial superoxide dismutase, cytosolic malic enzyme, xanthine oxidase. Fructose-biphosphate aldolase-2 and cytosolic aspartate aminotransferase possibly form a fifth LG. Mitochondrial aconitate hydratase, α-glucosidase,

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Parente, Lucas Leimig Telles, Rodrigo Emmanuel Leimig Telles Parente, Maria Valéria Leimig Telles, and Maria das Graças Nascimento Silva. "HEREDITARY FRUCTOSE INTOLERANCE IN A PEDIATRIC CONTEXT." Amadeus International Multidisciplinary Journal 3, no. 5 (2018): 66–74. http://dx.doi.org/10.14295/aimj.v3i5.51.

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Carbohydrate intolerance is relatively common in childhood, but its diagnosis and management are still quite precarious. Hereditary fructose intolerance (HFI) is an autosomal recessive disease that results in deficiency of the enzyme aldolase B, which contributes to the onset of gastrointestinal and metabolic symptoms, triggered by the ingestion of foods high in fructose, sucrose or sorbitol. Methodology: For the accomplishment of such a study a search of the literature was done from August to September of the year 2018 with publication period of a maximum of 10 years. The theoretical referenc

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