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these results pinpoint transaldolase as a novel metabolic enzyme possessing synthetic lethality with HER2 inhibition.
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These results demonstrate that the nucleocytoplasmic distribution of TALDO1, modulated via alternative translational initiation and dimer formation, plays an important role in a wide range of metabolic networks
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The above findings support the premise that biallelic mutations in TALDO1 are responsible for transaldolase deficiency and confirm the broad phenotypic variability of this condition, even with the same genotype.
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This study expands the clinical definition of transaldolase deficiency, and adds to its allelic heterogeneity.
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Data suggest that exchange reactions during gluconeogenesis catalyzed by transaldolase and triose-phosphate isomerase do not differ between subjects with type 2 diabetes and control subjects under fasting or hyperglycemic conditions.
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renal phenotype of patients with transaldolase deficiency
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these data provide strong experimental evidence that transaldolase exchange occurs in humans, resulting in an overestimate of gluconeogenesis
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Data show that erythronic acid was identified as a major abnormal metabolite in all patients and in knock-out TALDO mice implicating an as yet unknown biochemical pathway in this disease.
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granzyme B-cleaved transaldolase-specific T cell-mediated cytotoxicity may contribute to the progressive destruction of oligodendrocytes in patients with multiple sclerosis
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transaldolase is regulated by ZNF143 in a tissue-specific manner
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TALase undergoes anterograde trafficking in neutrophils from nonpregnant individuals, whereas retrograde trafficking is found during pregnancy
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Mutation in the TALDO1 gene was found in patients with hydrops fetalis and neonatal multi-organ disease.
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A patch of functionally important amino acid residues extends from serine-171 toward the catalytic site and is proposed as a novel ligand shuttling path connecting these specific sites to the enzyme's active site.
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Transaldolase-deficient patients had significantly increased urinary heptoses, revealing novel urinary biomarkers for identification of the deficiency.
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A new case of TALDO deficiency resulted in cirrhosis, rickets and deafness.
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The present study identified the TAL deficiency as a modulator of mitochondrial homoeostasis, Ca(2+) fluxing and apoptosis.
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analysis of enzymes TalB and Taldo1 in human and E. coli
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genetic polymorphisms in Transaldolase 1 are associated with squamous cell carcinoma of the head and neck .
