Cytosolic 5'-nucleotidase 3A (NT5C3A)

Cytosolic 5'-nucleotidase 3A (NT5C3A) is an **enzyme** of the 5'-nucleotidase family that catalyzes the dephosphorylation of pyrimidine nucleoside monophosphates, primarily uridine monophosphate (UMP) and cytidine monophosphate (CMP), as well as modified nucleotides like 7-methylguanosine monophosphate[1][2][3]. This activity is important for nucleotide catabolism, particularly during erythrocyte maturation and mRNA turnover. NT5C3A contributes to regulating the balance of endogenous nucleotides and responses to chemotherapeutic pyrimidine analogs (e.g., gemcitabine, cytarabine). Deficiency or mutation in this enzyme causes pyrimidine 5'-nucleotidase deficiency, a rare hereditary nonspherocytic hemolytic anemia. NT5C3A activity is inducible by interferons, and beyond its metabolic action, it participates in anti-inflammatory feedback loops by promoting epigenetic silencing of proinflammatory cytokine genes through NAD+-dependent sirtuin activation and NF-κB signaling suppression[5]. Genetic variants and expression levels of NT5C3A affect drug response and disease severity in hematologic disorders and cancers[1][2][3]. **Note:** The molecule is sometimes referenced as cytosolic 5'-nucleotidase 3 (NT5C3), but "A" designates the primary human isoform relevant for most clinical and biological contexts[1][2][3].

Other names

5'-nucleotidase, cytosolic IIIANT5C3ANT5C3Cytosolic 5'-nucleotidase 3ACytosolic 5'-nucleotidase 3Cytosolic 5'-nucleotidase IIIP5N1P5N-1PN-IUMPH1UMPHPSN1POMP7-methylguanosine nucleotidase7-methylguanosine phosphate-specific 5'-nucleotidaselupinp36EC 3.1.3.91EC 3.1.3.5

Dephosphorylation and inactivation of nucleoside analogs (e.g., cytarabine, gemcitabine), resulting in altered drug efficacy and chemoresistance in cancer therapy[1][2][3].