RRM2B / P53R2抗体

RRM2B / P53R2抗体产品信息

免疫原 :
Recombinant Human RRM2B / P53R2 protein (Catalog#13150-H07E)
Antibody Type : Rabbit Polyclonal Antibody ( Antibody Purification Platform )
抗体宿主 :
Rabbit IgG
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 :
Produced in rabbits immunized with purified, recombinant Human RRM2B / P53R2 (rh RRM2B / P53R2; Catalog#13150-H07E; Q7LG56-1; Met 1-Phe 351). RRM2B / P53R2 specific IgG was purified by Human RRM2B / P53R2 affinity chromatography.
RRM2B / P53R2抗体Background
Ribonucleoside reductase subunit M2B (also known as RRM2B or p53R2) is an enzyme belonging to the iron-dependent ribonucleotide reductase (RNR) enzyme family which is essential for DNA synthesis. Ribonucleotide reductase (RNR) is an enzyme that catalyzes the formation of deoxyribonucleotides from ribonucleotides and plays a critical role in regulating the total rate of DNA synthesis so that DNA to cell mass is maintained at a constant ratio during cell division and DNA repair. Using in vivo 32P-orthophosphate labeling, it has been observed that 32P can be incorporated into RRM2B/p53R2 induced by UV irradiation, suggesting that p53R2 is a phosphorylated protein. It is hypothesized that p53R2 activity can be regulated at the posttranslational level in response to DNA damage. p53R2 has previously been shown to be essential for the maintenance of mtDNA copy number and its candidacy for tumor suppression has been evaluated in several mutational analyses of different cancer types. However, the contribution of p53R2 to the DNA damage response has been questioned because its transcriptional induction upon DNA damage is not rapid enough for prompt DNA repair. Instead, ATM-mediated phosphorylation has been suggested to regulate the DNA repair activity of p53R2 posttranslationally. In addition, a defect in p53R2 can induce a mild muscle disease of adult onset through disturbance of mitochondrial homeostasis but that this defect does not appear to be oncogenic.
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