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Recombinant human XPC
Xeroderma pigmentosum complementation group C; DNA repair protein complementing XP C cells; DNA repair protein complementing XP-C cells; DNA repair protein complementing XPC cells; p125; RAD4; Xeroderma pigmentosum group C complementing protein; Xeroderma pigmentosum group C protein; Xeroderma pigmentosum group C-complementing protein; Xeroderma pigmentosum group III; XP 3; XP C; XP group C; XP3; Xpc; XPC gene; XPC_HUMAN; XPCC.
濃度：1mg/ ml
來源：Recombinant Human
純度：≥95% SDS-PAGE
表達系統(tǒng)：Escherichia coli
標簽：His tag
蛋白長度：Full length protein
內(nèi)毒素水平：<1.000 Eu/µg
純化方法：HPLC
應用：SDS-PAGE，Western blot，ELISA
Biological activity,immunology research
保存：-20℃
保質(zhì)期：1年
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.
多克隆抗體
產(chǎn)品名稱：Rabbit Anti-XPC antibody
Rabbit Anti-XPC
別名：Xeroderma pigmentosum complementation group C; DNA repair protein complementing XP C cells; DNA repair protein complementing XP-C cells; DNA repair protein complementing XPC cells; p125; RAD4; Xeroderma pigmentosum group C complementing protein; Xeroderma pigmentosum group C protein; Xeroderma pigmentosum group C-complementing protein; Xeroderma pigmentosum group III; XP 3; XP C; XP group C; XP3; Xpc; XPC gene; XPC_HUMAN; XPCC.
來源：Rabbit
克隆類型：Polyclonal
濃度：1mg/ml
亞型：IgG
反應：Human,Mouse,Rat (predicted: Pig,Cow,Horse)
應用： WB=1:1000-1:2000,Elisa=1:1000-1:2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500
理論分子量：106kDa
免疫原：KLH conjugated synthetic peptide derived from human XPC
保存：-20℃
保質(zhì)期：1年
單克隆抗體
產(chǎn)品名稱：Anti-XPC antibody
Mouse Anti-XPC
別名：Xeroderma pigmentosum complementation group C; DNA repair protein complementing XP C cells; DNA repair protein complementing XP-C cells; DNA repair protein complementing XPC cells; p125; RAD4; Xeroderma pigmentosum group C complementing protein; Xeroderma pigmentosum group C protein; Xeroderma pigmentosum group C-complementing protein; Xeroderma pigmentosum group III; XP 3; XP C; XP group C; XP3; Xpc; XPC gene; XPC_HUMAN; XPCC.
來源：Mouse
克隆類型：Monoclonal
濃度：1mg/ml
亞型：IgG
反應：Human
應用： WB=1:1000-1:2000,Elisa=1:1000-1:2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500
反應: Human
理論分子量：106kDa
免疫原：KLH conjugated synthetic peptide derived from human XPC
保存：-20℃
保質(zhì)期：1年
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.
