Ribonucleotide reductase regulatory TP53-inducible subunit M2B (RRM2B)

Ribonucleotide reductase regulatory TP53-inducible subunit M2B (RRM2B) is a small, p53-inducible subunit of ribonucleotide reductase (RNR), a critical enzyme catalyzing the conversion of ribonucleoside diphosphates to deoxyribonucleoside diphosphates, providing the building blocks for DNA synthesis and repair[1][2][3][4]. In response to DNA damage or cellular stress, RRM2B replaces the standard RNR small subunit to form a complex essential for DNA repair, maintenance of both nuclear and mitochondrial DNA, and cellular responses to oxidative stress. Deficiency in RRM2B impairs mitochondrial DNA maintenance and is linked to mitochondrial depletion syndromes and specific inherited disorders, while genomic amplifications or altered expression have been described in several cancers, where RRM2B influences tumor progression, genomic integrity, and therapy response. Therapeutic targeting of RRM2B or its regulatory networks is an ongoing area of oncology and rare disease research[2][3][4].

Other names

Ribonucleoside-diphosphate reductase subunit M2 BP53R2p53R2TP53-inducible ribonucleotide reductase M2 Bp53-inducible ribonucleotide reductase small subunit 2-like proteinMTDPS8AMTDPS8BRCDFRDribonucleotide reductase M2 B (TP53 inducible)

Inhibition of ribonucleotide reductase reduces deoxyribonucleotide pools, thereby inhibiting DNA synthesis and repair, leading to cytostatic or cytotoxic effects in tumor cells