Mouse Xeroderma Pigmentosum, Complementation Group C (XPC) RTU ELISA Kit | XPC rtu elisa kit

Mouse Xeroderma Pigmentosum, Complementation Group C (XPC) ELISA Kit

Cat. Num. AAA4503412

• Reactivity: Mouse
• Synonyms: Xeroderma Pigmentosum; Complementation Group C (XPC); Mouse Xeroderma Pigmentosum; Complementation Group C (XPC) ELISA Kit; XP-C; XP3; XPCC; RAD4; Xeroderma Pigmentosum Group C Protein; DNA repair protein complementing XP-C cells; XPC rtu elisa kit

• Reactivity: Mouse
• Sequence Length: 930

• Assay Type: Sandwich
• Samples: Tissue Homogenates or Other Biological Fluids.
• Detection Range: 0.156-10ng/mL
• Sensitivity: 0.061ng/mL
• RTU ELISA Kit's Advantage: The Ready-To-Use (RTU) Kits require fewer steps in setup and take less time to run. Detection Solutions are pre-diluted and total incubation time is shorter than many other ELISA Kits.
• Preparation and Storage: For unopened kits: All the reagents should be kept at 4 degree C upon receipt.; For opened kits: Once the kit is opened, the remaining reagents still need to be stored according to the above storage conditions. In addition, return the unused wells to the foil pouch containing the desiccant pack and reseal along entire edge of zip-seal.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for XPC rtu elisa kit

Test Principle: The microtiter plate provided in this kit has been pre-coated with an antibody specific to XPC. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific to XPC. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain XPC, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of XPC in the samples is then determined by comparing the O.D. of the samples to the standard curve.

NCBI and Uniprot Product Information

• NCBI GI #: 121247429
• NCBI GeneID: 22591
• NCBI Accession #: NP_033557.2
• NCBI GenBank Nucleotide #: NM_009531.2
• UniProt Accession #: P51612; P54732; Q3TKI2; Q920M1; Q9DBW7
• Molecular Weight: 104,522 Da
• NCBI Official Full Name: DNA repair protein complementing XP-C cells homolog
• NCBI Official Synonym Full Names: xeroderma pigmentosum, complementation group C
• NCBI Official Symbol: Xpc
• NCBI Protein Information: DNA repair protein complementing XP-C cells homolog
• UniProt Protein Name: DNA repair protein complementing XP-C cells homolog
• Protein Family: DNA repair protein
• UniProt Gene Name: Xpc

Uniprot Description

Involved in global genome nucleotide excision repair (GG-NER) by acting as damage sensing and DNA-binding factor component of the XPC complex. Has only a low DNA repair activity by itself which is stimulated by Rad23b and Rad23a. Has a preference to bind DNA containing a short single-stranded segment but not to damaged oligonucleotides. This feature is proposed to be related to a dynamic sensor function: XPC can rapidly screen duplex DNA for non-hydrogen-bonded bases by forming a transient nucleoprotein intermediate complex which matures into a stable recognition complex through an intrinsic single-stranded DNA-binding activity.The XPC complex is proposed to represent the first factor bound at the sites of DNA damage and together with other core recognition factors, Xpa, RPA and the TFIIH complex, is part of the pre-incision (or initial recognition) complex. The XPC complex recognizes a wide spectrum of damaged DNA characterized by distortions of the DNA helix such as single-stranded loops, mismatched bubbles or single-stranded overhangs. The orientation of XPC complex binding appears to be crucial for inducing a productive NER. XPC complex is proposed to recognize and to interact with unpaired bases on the undamaged DNA strand which is followed by recruitment of the TFIIH complex and subsequent scanning for lesions in the opposite strand in a 5'-to-3' direction by the NER machinery. Cyclobutane pyrimidine dimers (CPDs) which are formed upon UV-induced DNA damage esacpe detection by the XPC complex due to a low degree of structural perurbation. Instead they are detected by the UV-DDB complex which in turn recruits and cooperates with the XPC complex in the respective DNA repair. In vitro, the Xpc:Rad23b dimer is sufficient to initiate NER; it preferentially binds to cisplatin and UV-damaged double-stranded DNA and also binds to a variety of chemically and structurally diverse DNA adducts. XPC:RAD23B contacts DNA both 5' and 3' of a cisplatin lesion with a preference for the 5' side. Xpc:Rad23b induces a bend in DNA upon binding. Xpc:Rad23b stimulates the activity of DNA glycosylases Tdg and Smug1 ().