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Transaldolase is a key enzyme in the non-oxidative phase of the pentose phosphate pathway (PPP), facilitating the reversible transfer of a three-carbon dihydroxyacetone moiety between sugar phosphates [UniProt: P37837]. By connecting the PPP to glycolysis, it plays a vital role in regulating the supply of ribose-5-phosphate for nucleotide synthesis and maintaining cellular NADPH levels, which are essential for antioxidant defense and reductive biosynthesis [PubMed: 15103320]. Clinically, transaldolase deficiency is a rare autosomal recessive metabolic disorder that presents with liver cirrhosis, hepatosplenomegaly, and hemolytic anemia [OMIM: 606003]. In the context of oncology, transaldolase is frequently overexpressed in various tumors, where it supports metabolic reprogramming and provides resistance to oxidative stress-induced apoptosis [PubMed: 26437224]. Furthermore, it has been identified as a candidate autoantigen in multiple sclerosis, suggesting a role in autoimmune pathogenesis [PubMed: 12637434]. While no direct pharmacological inhibitors are currently in clinical use, transaldolase represents a promising target for metabolic intervention in cancer and autoimmune conditions.
Catalyzes the reversible transfer of a three-carbon dihydroxyacetone moiety from sedoheptulose-7-phosphate to glyceraldehyde-3-phosphate to form erythrose-4-phosphate and fructose-6-phosphate [UniProt: P37837].
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