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RRM2B / P53R2 Antibody, Mouse MAb

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RRM2B/P53R2Antibody Product Information
Immunogen:Recombinant Human RRM2B / P53R2 protein (Catalog#13150-H07E)
Clone ID:04
Ig Type:Mouse IgG1
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation:This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human RRM2B / P53R2 (rh RRM2B / P53R2; Catalog#13150-H07E; Q7LG56-1; Met 1-Phe 351). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
RRM2B/P53R2Antibody Usage Guide
Specificity:Human RRM2B / P53R2
No cross-reactivity in ELISA with
E.coli cell lysate
Application:WB, ELISA

WB: 20-30 μg/ml

ELISA: 0.5-1 μg/mL

This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human RRM2B. The detection limit for Human RRM2B is approximately 0.039 ng/well.

Storage:This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

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. RRM2B is a phosphorylated protein. It is hypothesized that RRM2B activity can be regulated at the posttranslational level in response to DNA damage. RRM2B 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 RRM2B 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 RRM2B posttranslationally. In addition, a defect in RRM2B can induce a mild muscle disease of adult onset through disturbance of mitochondrial homeostasis but that this defect does not appear to be oncogenic. 

  • Bourdon A, et al. (2007) Mutation of RRM2B, encoding p53-controlled ribonucleotide reductase (p53R2), causes severe mitochondrial DNA depletion. Nature Genetics. 39: 776-80.
  • Tyynismaa H, et al. (2009) A Heterozygous Truncating Mutation in RRM2B Causes Autosomal-Dominant Progressive External Ophthalmoplegia with Multiple mtDNA Deletions. AJHG. 85 (2) : 290-5.
  • Shaibani A, et al. (2009) Mitochondrial neurogastrointestinal encephalopathy due to mutations in RRM2B. Arch Neurol.66 (8): 1028-32.
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