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Human Ribonucleoside-Diphosphate Reductase Subunit M2 B (RRM2B) ELISA Kit
Human Ribonucleoside-Diphosphate Reductase Subunit M2 B (RRM2B) ELISA Kit
This ELISA kit is designed to detect Human Ribonucleoside-Diphosphate Reductase Subunit M2 B (Human RRM2B). The assay plate has been pre-coated with mouse anti-Human p53R2 monoclonal antibody. When the sample containing p53R2 is added to the plate, it binds to the antibodies coated on the wells. Then, a horseradish peroxidase conjugated mouse anti-Human p53R2 Antibody is added to the wells and binds to p53R2 in the sample. After washing the wells, substrate solutions are added, and the color intensity is directly proportional to the amount of Human p53R2 present. The reaction is stopped by adding an acidic stop solution, and the absorbance is measured at 450 nm.
Catalog No:
BPE266
Regular price
$754.00 USD
Regular price
$580.00 USD
Sale price
$754.00 USD
Unit price
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per
2 weeks
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Product Details
Species Reactivity
Human
Sensitivity
14.93 pg/mL
Detection Range
46.88-3000 pg/mL
Sample Type
Serum, plasma, cell culture supernates
Incubation(s)
3.5 hour(s)
Research Areas
Cancer, Epigenetics and Nuclear Signaling, Metabolism
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. Besides, 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.
Shipping Condition
Shipped on cold gel packs.
Storage Condition and Shelf Life
This product can be stored at 2-8C.
Analyte
Ribonucleoside-diphosphate reductase subunit M2 B
Regulatory Status
For Research Use Only
