Literature summary for 1.17.4.1 extracted from

Pontarin, G.; Ferraro, P.; Bee, L.; Reichard, P.; Bianchi, V.
Mammalian ribonucleotide reductase subunit p53R2 is required for mitochondrial DNA replication and DNA repair in quiescent cells (2012), Proc. Natl. Acad. Sci. USA, 109, 13302-13307.

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Application

Application	Comment	Organism
medicine	skin fibroblasts isolated from a patient with a lethal homozygous missense mutation of ioform p53R2 grow normally in culture with an unchanged complement of mtDNA. During active growth, the four dNTP pools do not differ in size from normal controls, whereas during quiescence, the dCTP and dGTP pools decrease to 50% of the control. On withdrawal of ethidium bromide depleting cell of mitochondrial DNA, mitochondrial DNA recovers equally well in cycling mutant and control cells, whereas during quiescence, the mutant fibroblasts remain deficient. Addition of deoxynucleosides to the medium increases intracellular dNTP pools and normalizes mtDNA synthesis. Quiescent mutant fibroblasts are also deficient in the repair of UV-induced DNA damage	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q7LG56	isoform p53R2	-

Synonyms

Synonyms	Comment	Organism
ribonucleoside-diphosphate reductase subunit M2 B	-	Homo sapiens

General Information

General Information	Comment	Organism
physiological function	in nontransformed cells only during quiescence, isoform p53R2 is required for maintenance of mitochondrial DNA and for optimal DNA repair after UV damage	Homo sapiens

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Release 2023.1 (January 2023)