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Human RRM2B / P53R2 ELISA Pair Set

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Human RRM2B/P53R2 Materials provided
Capture Ab:0.5 mg/mL of mouse anti-RRM2B monoclonal antibody. Dilute to a working concentration of 2 μg/mL in CBS before coating.
Detection Ab:0.5 mg/mL mouse anti-RRM2B monoclonal antibody conjugated to horseradish-peroxidase (HRP). Dilute to working concentration of 0.5 μg/mL in detection antibody dilution buffer before use.
Standard:Each vial contains 63 ng of recombinant RRM2B. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20℃ to -80℃ in a manual defrost freezer. A seven-point standard curve using 2-fold serial dilutions in sample dilution buffer, and a high standard of 3 ng/mL is recommended.
Human RRM2B/P53R2 Specificity
Human RRM2B/P53R2 Sensitivity
The minimum detectable dose of Human RRM2B / P53R2 was determined to be approximately 47 pg/ml. This is defined as at least three times standard deviations above the mean optical density of 10 replicates of the zero standard.
Human RRM2B/P53R2 Principle of the product
The Human RRM2B / P53R2 ELISA Pair Set is for the quantitative determination of Human RRM2B / P53R2.
This ELISA Pair Set contains the basic components required for the development of sandwich ELISAs.
The Sino Biological ELISA Pair Set is a solid phase sandwich ELISA (Enzyme-Linked Immunosorbent Assay). It utilizes a monoclonal antibody specific for RRM2B / P53R2 coated on a 96-well plate. Standards and samples are added to the wells, and any RRM2B / P53R2 present binds to the immobilized antibody. The wells are washed and a horseradish peroxidase conjugated mouse anti-RRM2B / P53R2 monoclonal antibody is then added, producing an antibody-antigen-antibody “sandwich”. The wells are again washed and TMB substrate solution is loaded, which produces color in proportion to the amount of RRM2B / P53R2 present in the sample. To end the enzyme reaction, the stop solution is added and absorbances of the microwell are read at 450 nm.
Human RRM2B/P53R2 Storage
Capture Antibody: Aliquot and store at -20℃ to -80℃ for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Detection Antibody: Protect it from prolonged exposure to light. Aliquot and store at -20℃ to -80℃ and for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Standard: Store lyophilized Standard at -20℃ to -80℃ for up to 6 months from date of receipt. Aliquot and store the reconstituted Standard at -80℃ for up to 1 month. Avoid repeated freeze-thaw cycles.
RRM2B/P53R2 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. 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. 

Human RRM2B/P53R2 References
  • 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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    • Human RRM2B / P53R2 ELISA standard curve