You dont need to know this in humans the complex is

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Unformatted text preview: (such as uracil glycosylase) gets rid of the base, all mistakes are fixed by a common pathway: AP endonuclease nicks 5’ of the abasic site  ­> Phosphodiesterase cleaves the backbone to get rid of the nt  ­> DNA PolI fills in the gap  ­> ligase seals the nick 3. Nucleotide excision repair (NER): specific enzymes are UvrAB complex, UvrC excinuclease and UvrD helicase (shared with mismatch repair)  ­ ­> example mistake would be pyramidine dimers or other intrastrand cross links that distort B ­DNA  ­ ­> one strand is saved as a template  ­ ­> UvrA/B marks the spot, and UvrC cleaves at 5’ and 3’ of the lesion  ­ ­> the displaced strand (by UvrD helicase activity) is a specific length because of the size of the UvrAB complex: bacteria ­12bp; humans ­29bp  ­ ­> then PolI and ligase are used to fix the gap, no need for SSB since the displaced strand is small (although in humans, RPA is required because the displaced strand is bigger; you don’t need to know this)  ­ ­> in humans, the complex is called XP complex, where XPA/C are UvrAB equivalents, XPB/D are helicases, thus UvrD...
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