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- W72459652 abstract "Purine nucleoside phosphorylase (PNP:EC 2.4.2.1) deficiency appears to result in a predominantly T cell immune defect1. Lack of the PNP enzyme leads to the inability to degrade deoxynucleosides, particularly deoxyguanosine (dGR) resulting in the intracellular accumulation of deoxyguanosine triphosphate (dGTP) which is known to inhibit DNA synthesis in vitro2. Deoxycytidine kinase is considered responsible for the initial conversion of dGR to dGMP1. Hence deoxycytidine (dCR), the preferred substrate, should competitively inhibit dGTP accumulation as has been demonstrated in vitro1,2. However, oral dCR therapy for six months in a PNP deficient child produced no clinical or immunological improvement, probably due to degradation in the gut or rapid deamination3." @default.
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- W72459652 date "1984-01-01" @default.
- W72459652 modified "2023-09-27" @default.
- W72459652 title "Purine Nucleoside Phosphorylase (PNP) Deficiency: A Therapeutic Challenge" @default.
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- W72459652 doi "https://doi.org/10.1007/978-1-4684-4553-4_10" @default.
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