Entry of XPG to PIC is accompanied by departure of XPC from the complex. However, it is doubtful that XPC protein plays a direct role in recruiting XPG because PIC where PIC does not actually contain XPC but otherwise is similar to regular PIC in the sense of having XPA, RPA, TFIIH, and unwound DNA.XPG is known to interact with TFIIH specifically and it is most likely that it is recruited to PIC by TFIIH.The failure to detect XPC in PIC by supershift assays provides direct experimental evidence of this step.Preincision Complex The XPFzERCC complex is re Damage Recognition in Excision Repair. Biol. Chem. doi. jbc. Access the most updated version of this article at http:www.jbc.orgcontent When a correction for this article is posted Click here to choose from all of JBCs email alerts This article cites references, of which can be accessed free at http:www.jbc.orgcontent.full.htmlreflist Downloadedfromhttp: www.jbc.orgbyguestonSeptember, It is comprised of two subpathways: transcriptioncoupled repair that accomplishes efficient removal of damage blocking transcription and global genome repair.Recently, the basic mechanism of global genome repair has emerged from biochemical studies.However, little is known about transcriptioncoupled repair in eukaryotes.Here we report the identification of a novel protein designated XAB that was identified by virtue of its ability to interact with XPA, a factor central to both nucleotide excision repair subpathways.The XAB protein of amino acids consists mainly of tetratricopeptide repeats.In addition to interacting with XPA, immunoprecipitation experiments demonstrated that a fraction of XAB is able to interact with the transcriptioncoupled repairspecific proteins CSA and CSB as well as RNA polymerase II.Furthermore, antibodies against XAB inhibited both transcriptioncoupled repair and transcription in vivo but not global genome repair when microinjected into living fibroblasts.These results indicate that XAB is a novel component involved in transcriptioncoupled repair and transcription.NER is a highly versatile and strongly conserved DNA damage repair pathway.The costs of publication of this article were defrayed in part by the payment of page charges.The importance of NER is highlighted by the clinical features of rare human hereditary conditions caused by a deficiency in NER, such as xeroderma pigmentosum. XP patients show striking hypersensitivity to sunlight and an extremely high incidence of skin cancer in sunexposed areas and frequently progressive neurological degeneration.CS patients show photohypersensitivity, cachectic dwarfism, and severe mental retardation but, unlike XP patients, no predisposition to skin cancer. Two genetic complementation groups exist: CSA and CSB.In contrast to XPC, the defect within CS is restricted to TCR. To date, all of the known genes responsible for XP and CS. Recently, the core reaction of NER in humans has been reconstituted in vitro with purified proteins. The XPCHRB complex is the main factor to initiate global genome repair by sensing and binding to <a href="http://www.molbioglobal.com/archives/283"></a>
various types of lesion. The UVDDB protein complex that is affected in XPE patients is required for recognition of a specific subset of damage, such as cyclobutane pyrimidine dimers. The binding of XPCHRB complex to a lesion presumably induces a conformational change in the DNA around the injury.TFIIH, a general transcription initiation factor containing the XPB and XPD DNA helicases, is recruited to the recognized injury and locally unwinds the DNA duplex by its bidirectional DNA helicase activities to form an open reaction intermediate.