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- Table of Contents
Information about Fructose-1,6-diphosphatase Deficiency: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Most recent studies have shown that Fructose-1,6-diphosphatase Deficiency shares some biological mechanisms with acidemia, acidosis, acidosis-lactic, ataxia, deficiency-of-fructokinase, galactosemias, glycogen-storage-disease, glycogen-storage-disease-type-i, hepatomegaly, hereditary-fructose-intolerance-syndrome, hypoglycemia, inborn-errors-of-metabolism, infective-disorder, ketosis, liver-diseases, metabolic-acidosis, metabolic-diseases, propionic-acidemia, pyruvate-dehydrogenase-complex-deficiency-disease.
Among the many pathways, these few ones have gauged particular interests from scientists studying Fructose-1,6-diphosphatase Deficiency, and have been seen in publications frequently: Coagulation, Excretion, Fatty Acid Oxidation, Glucagon Secretion, Gluconeogenesis, Glucose Homeostasis, Glycolysis, Localization, Pathogenesis, Pyruvate Oxidation, Secretion, Translation, Urea Cycle
Quite a number of genes have been found to play important roles in Fructose-1,6-diphosphatase Deficiency, such as FBP1, FOLR1, FOLR2, FUBP1, G6PC, G6PD, GALK1, GCG, GK, GSTP1, INS, OVGP1, PC, QPCT, RAB14, TGM2, UBL4A. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.
Coagulation | Excretion | Fatty Acid Oxidation |
Glucagon Secretion | Gluconeogenesis | Glucose Homeostasis |
Glycolysis | Localization | Pathogenesis |
Pyruvate Oxidation | Secretion | Translation |
Urea Cycle |