This antibody solution is provided at a concentration of 1mg/ml and is formulated in a buffer consisting of PBS at pH 7.4, 10% glycerol, and 0.02% sodium azide.
This antibody has undergone rigorous testing in various applications, including ELISA, Western blot analysis, and immunocytochemistry/immunofluorescence (ICC/IF), to ensure its specificity and reactivity. As optimal working dilutions may vary depending on the specific application and experimental conditions, it is recommended to perform a titration to determine the most effective concentration for your experiment.
PAT71H3AT.
Anti-human XPA mAb, clone PAT71H3, is derived from hybridization of mouse F0 myeloma cells with spleen cells from BALB/c mice immunized with a recombinant human XPA protein 1-273 amino acids purified from E. coli.
Mouse IgG1 heavy chain and k light chain.
Xeroderma Pigmentosum (XP) is a rare autosomal recessive disorder characterized by extreme sensitivity to ultraviolet (UV) rays from sunlight, with a high predisposition to skin cancers and, in some cases, neurological abnormalities . The disease is caused by defects in the nucleotide excision repair (NER) pathway, which is responsible for repairing UV-induced DNA damage .
XPA is one of the seven complementation groups (A-G) of XP, each corresponding to a different gene involved in the NER pathway . The XPA gene encodes a protein that plays a crucial role in the NER process by verifying DNA damage and stabilizing the repair complex . Mutations in the XPA gene lead to a defective NER pathway, resulting in the accumulation of unrepaired DNA damage and increased mutagenesis .
The mouse anti-human XPA antibody is a monoclonal antibody developed to target the human XPA protein. This antibody is used in various research applications, including immunofluorescence, Western blotting, and immunoprecipitation, to study the expression and function of the XPA protein in human cells .
Research involving the XPA protein and its corresponding antibody has provided significant insights into the mechanisms of DNA repair and the pathogenesis of XP. For instance, studies have shown that the XPA protein is essential for repairing clustered oxidative DNA adducts, which are complex forms of DNA damage caused by ionizing radiation . Additionally, the mouse anti-human XPA antibody has been used to investigate the localization and function of the XPA protein in various cell types .
Current therapeutic approaches for XP primarily focus on preventing UV exposure and managing skin cancers. However, recent research has explored novel strategies to enhance DNA repair and reduce the disease burden. For example, specific sulfonylureas have been shown to promote the clearance of DNA damage and increase resistance to UV radiation in cellular models of XP . Moreover, nicotinamide and caloric restriction have demonstrated potential in attenuating the effects of UV radiation and decreasing DNA damage burden in animal models .