DNA Damage Quantification Kit-AP Site Counting-

DNA Damage Quantification Kit-AP Site Counting-

Catalog Number:
CFA1108130DOJ
Mfr. No.:
DK02-12
Price:
$768
  • Size:
    20 samples
    Quantity:
    Add to Cart:
      • Overview
        • Oxidative damage to DNA is a result of its interaction with reactive oxygen species (ROS), in particular, the hydroxy radical. Hydroxy radicals, which are produced from superoxide anion and hydrogen peroxide by the Fenton reaction, produce multiple modifications in DNA. Oxidative attacks by hydroxy radicals on the deoxyribose moiety will lead to the release of free bases from DNA, generating strand breaks with various sugar modifications and simple abasic sites (AP sites). In fact, AP sites are one of the major types of damage generated by ROS. Aldehyde Reactive Probe (ARP; N'-aminooxymethylcarbonylhydrazin-D-biotin) reacts specifically with an aldehyde group present on the open ring form of the AP sites. This reaction makes it possible to detect DNA modifications that result in the formation of an aldehyde group. After treatment with excess ARP reagent, all of the AP sites on DNA are tagged with a biotin residue. These biotin-tagged AP sites can be quantified using the avidin-biotin assay, followed by colorimetric detection with either peroxidase or alkaline phosphatase conjugated to the avidin. DNA Damage Quantification Kit contains all the necessary solutions for detecting between 1 to 40 AP sites per 1 x 105 base pairs.

          Please contact us at for specific academic pricing.

      • Properties
        • Categories
          SOD Activity, Glutathione, DNA Damage, Antioxidant capacity
          Storage
          0-5°C
          Shipping
          with blue ice

          * For research use only

      • Reference
        • 1) T. Lindahl, et al., Rate of Depurination of Native Deoxyribonucleic Acid. Biochemistry. 1972;11:3610-3618.

          2) M. Liuzzi, et al., A New Approach to the Study of the Base-excision Repair Pathway Using Methoxyamine. J Biol Chem. 1985;260:5252-5258.

          3) A. Sancar, et al., DNA Repair Enzymes. Annu Rev Biochem. 1988;57:29-67.

          4) M. Weinfeld, et al., Response of Phage T4 Polynucleotide Kinase Toward Dinucleotides Containing Apurinic Sites: Design of a 32P-postlabeling Assay for Apurinic Sites in DNA. Biochemistry. 1990;29:1737-1743.

          5) B. X. Chen, et al., Properties of a Monoclonal Antibody for the Detection of Abasic Sites, a Common DNA Lesion. Mutat Res. 1992;273:253-261.

          6) J. A. Gralnick, et al., The YggX Protein of Salmonella enterica Is Involoved in Fe(II) Trafficking and Minimizes the DNA Damage Cause by Hydroxyl Radicals:Residue CYS-7 is Essential for YggX Function. J Biol Chem. 2003;278:20708-20715.

          7) J. W. Pippin, et al., DNA Damage is a Novel Response to Sublytic Complement C5b-9 Induced Injury in Podocytes. J Clin Invest. 2003;111:877-885.

          8) S. Watanabe, et al., Methylated DNA-binding Domain 1 and Methylpurine DNA Glycosylase Link Transcriptional Repression and DNA Repair in Chromatin. PNAS. 2003;100:12859-12864.

          9) M. Endres, et al., Folate Deficiency Increases Postischemic Brain Injury. Stroke. 2005;36:321-325.

          10) J. Li, et al., Angiotensin II-Induced Neural Differentiation via Angiotensin II Type 2 (AT2) Receptor-MMS2 Cascade Involving Interaction between AT2 Receptor-Interacting Protein and Src Homology 2 Domain-Containing Protein-Tyrosine Phosphatase 1. Mol Endocrinol. 2007;21:499-511.

          11) D. R. McNeill, et al., A Dominant-Negative Form of the Major Human Abasic Endonuclease Enhances Cellular Sensitivity to Laboratory and Clinical DNA-Damaging Agents. Mol Cancer Res. 2007;5:61-70.

          12) C. A. Downs, et al., Cellular pathology and histopathology of hypo-salinity exposure on the coral Stylophora pistillata. Sci Total Environ. 2009;407:4838-4851.

          13) C. A. Downs, et al., Symbiophagy as a cellular mechanism for coral bleaching. Autophagy. 2009;5:211-216.

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