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Aldolase B, fructose-bisphosphate

ALDOB, Aldo-2
Fructose-1,6-bisphosphate aldolase (EC is a tetrameric glycolytic enzyme that catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. Vertebrates have 3 aldolase isozymes which are distinguished by their electrophoretic and catalytic properties. Differences indicate that aldolases A, B, and C are distinct proteins, the products of a family of related 'housekeeping' genes exhibiting developmentally regulated expression of the different isozymes. The developing embryo produces aldolase A, which is produced in even greater amounts in adult muscle where it can be as much as 5% of total cellular protein. In adult liver, kidney and intestine, aldolase A expression is repressed and aldolase B is produced. In brain and other nervous tissue, aldolase A and C are expressed about equally. There is a high degree of homology between aldolase A and C. Defects in ALDOB cause hereditary fructose intolerance. [provided by RefSeq, Dec 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, POLYMERASE, Orosomucoid
Papers on ALDOB
Hereditary Fructose Intolerance
Weisfeld-Adams et al., Seattle, United States. In Unknown Journal, Jan 2016
DIAGNOSIS/TESTING: The diagnosis of HFI is established in a proband (with suggestive metabolic disturbances and clinical findings following dietary exposure to fructose, sucrose, or sorbitol) who has demonstrated either biallelic pathogenic variants in ALDOB on molecular genetic testing or deficient hepatic fructose 1-phosphate aldolase (aldolase B) activity on liver biopsy.
Threonine modulates immune response, antioxidant status and gene expressions of antioxidant enzymes and antioxidant-immune-cytokine-related signaling molecules in juvenile blunt snout bream (Megalobrama amblycephala).
Chen et al., Wuxi, China. In Fish Shellfish Immunol, Dec 2015
Dietary Thr regulated the gene expressions of Cu/Zn-SOD, Mn-SOD and CAT, GPx1, glutathione S-transferase mu (GST), nuclear factor erythroid 2-related factor 2 (Nrf2), heat shock protein-70 (Hsp70), tumour necrosis factor-alpha (TNF-α), apolipoprotein A-I (ApoA1), glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and fructose-bisphosphate aldolase B (ALDOB); while the gene expression of peroxiredoxin II (PrxII) was not significantly modified by graded Thr levels.
Aldolase-B knockout in mice phenocopies hereditary fructose intolerance in humans.
Tolan et al., Boston, United States. In Mol Genet Metab, Mar 2015
A serious defect of fructose metabolism is the autosomal recessive condition called hereditary fructose intolerance (HFI), caused by mutations in the human aldolase B gene (Aldob).
Molecular Diagnosis of Hereditary Fructose Intolerance: Founder Mutation in a Community from India.
Verma et al., New Delhi, India. In Jimd Rep, 2014
This leads to much delay in diagnosis with consequent harm to the patient.We report mutations in the ALDOB gene, from eleven Indian patients, seven of whom belong to the Agarwal community.
Aldolase B inhibits metastasis through Ten-Eleven Translocation 1 and serves as a prognostic biomarker in hepatocellular carcinoma.
Zhou et al., Shanghai, China. In Mol Cancer, 2014
BACKGROUND: Downregulation of Aldolase B (ALDOB) has been reported in hepatocellular carcinoma.
Analysis and interpretation of transcriptomic data obtained from extended Warburg effect genes in patients with clear cell renal cell carcinoma.
Diehl et al., Switzerland. In Oncoscience, 2014
Genes that are highly under-expressed include ALDOB, PKLR, PFKFB2, G6PC, PCK1, FBP1, PC, and SUCLG1.
Mitochondrial-related proteomic changes during obesity and fasting in mice are greater in the liver than skeletal muscles.
Ostrowski et al., Warsaw, Poland. In Funct Integr Genomics, 2014
The network centered on cytochromes P450 3a11 (Cyp3a11) and 4a14 (Cyp4a14), and fructose-bisphosphate aldolase B (Aldob) proteins which bridged proteins cluster involved in Metabolism of xenobiotics with proteins engaged in Fatty acid metabolism and PPAR signaling pathways.
ALDOB acts as a novel HBsAg-binding protein and its coexistence inhibits cisplatin-induced HepG2 cell apoptosis.
Guleng et al., Xiamen, China. In Crit Rev Eukaryot Gene Expr, 2013
We previously screened fructose-bisphosphate aldolase B (ALDOB) as a candidate binding protein of hepatitis B surface antigen (HBsAg) using a yeast 2-hybrid assay.
Electronic medical records and genomics (eMERGE) network exploration in cataract: several new potential susceptibility loci.
McCarty et al., Seattle, United States. In Mol Vis, 2013
The 45 SNPs associated with cataract at p<1×10(-5) are in several interesting genes, including ALDOB, MAP3K1, and MEF2C.
Aldolase positively regulates of the canonical Wnt signaling pathway.
Rosin-Arbesfeld et al., Tel Aviv-Yafo, Israel. In Mol Cancer, 2013
Here we report that ALDOC, Aldolase A (ALDOA) and Aldolase B (ALDOB) activate Wnt signaling in a GSK-3β-dependent mechanism, by disrupting the GSK-3β-Axin interaction and targeting Axin to the dishevelled (Dvl)-induced signalosomes that positively regulate the Wnt pathway thus placing the Aldolase proteins as novel Wnt signaling regulators.
Inhibition of hepatocyte nuclear factor 1 and 4 alpha (HNF1α and HNF4α) as a mechanism of arsenic carcinogenesis.
Hernandez et al., Barcelona, Spain. In Arch Toxicol, 2013
Results show a consistent down-regulation of HNF1α and HNF4α under a scenario of exposure where HepG2 cells (1) gained resistance to arsenic-induced toxicity/apoptosis, (2) attained loss of tissue-specific features (as shown by the observed down-regulation of ALDOB, PEPCK and CYP1A2, triggering of the epithelial-to-mesenchymal transition program and the hypersecretion of matrix metalloproteinase-2 and 9), (3) failed to maintain balanced expression of the "stemness" genes C-MYC, OCT3/4, LIN28 and NOTCH2 and (4) showed glucose metabolism impairment.
A Novel Frameshift Mutation of the ALDOB Gene in a Korean Girl Presenting with Recurrent Hepatitis Diagnosed as Hereditary Fructose Intolerance.
Yoo et al., Seoul, South Korea. In Gut Liver, 2012
Genetic analysis of ALDOB revealed that she is a homozygote for a novel frameshifting mutation c[758_759insT]+[758_759insT] (p.[val25 3fsX24]+[val253fsX24]).
Upregulation of aldolase B and overproduction of methylglyoxal in vascular tissues from rats with metabolic syndrome.
Wu et al., Saskatoon, Canada. In Cardiovasc Res, 2012
Upregulation of aldolase B by accumulated fructose is a common mechanism for methylglyoxal overproduction in vascular smooth muscle cella and aorta in different models of metabolic syndrome.
Integration of PCR-Sequencing Analysis with Multiplex Ligation-Dependent Probe Amplification for Diagnosis of Hereditary Fructose Intolerance.
Morrone et al., Florence, Italy. In Jimd Rep, 2011
Mutations in the ALDOB gene impair the activity of the hepatic aldolase B enzyme, causing hereditary fructose intolerance (HFI), an inherited autosomic recessive disease of carbohydrate metabolism, that can result in hypoglycemia, liver and kidney failure, coma, and death.
Stabilization of the predominant disease-causing aldolase variant (A149P) with zwitterionic osmolytes.
Tolan et al., Boston, United States. In Biochemistry, 2011
Aldolase B with the A149P substitution has activity that is <100-fold that of the wild type.
Screening and identification of differentially expressed genes in goose hepatocytes exposed to free fatty acid.
Lv et al., China. In J Cell Biochem, 2011
Meanwhile, 13 clones similar to the genes DGAT-1, ACSL1, DHRS7, PPARα, L-FABP, DGAT-2, PCK, ACSL3, CPT-1, A-FABP, PPARβ, MAT, and ALDOB had significantly higher expression levels in the hepatocytes treated with FFA mixtures.
Hereditary fructose intolerance: functional study of two novel ALDOB natural variants and characterization of a partial gene deletion.
Salvatore et al., Napoli, Italy. In Hum Mutat, 2010
This is the first report of six unrelated patients sharing the same ALDOB deletion, thus indicating a founder effect for this allele.
Mutations in the promoter region of the aldolase B gene that cause hereditary fructose intolerance.
Tolan et al., Boston, United States. In J Inherit Metab Dis, 2010
These novel mutations in ALDOB represent 2% of alleles in American HFI (hereditary fructose intolerance) patients, with IVS1+1G>C representing a significantly higher allele frequency (6%) among HFI patients of Hispanic and African-American ethnicity.
The biochemical basis of hereditary fructose intolerance.
Timson et al., Belfast, United Kingdom. In J Inherit Metab Dis, 2010
Biochemical study of defective aldolase B enzymes is key to revealing the molecular basis of the disease and providing a stronger basis for improved treatment and diagnosis
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