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. 2020 May 20;43(1 Suppl 1):e20190085. doi: 10.1590/1678-4685-GMB-2019-0085

Figure 1. Physical blockage of RNA polymerase II facilitates CSB binding to it. The following is responsible for recruiting p300, CSA and the other NER factors. CSA, together with CUL4, RBX1 and DDB1 are constantly ubiquitinating CSB, however UVSSA-USP7 complex are constantly removing ubiquitin tags from it. CSA also recruits HMGN1, which together with p300 unwinds chromatin upstream RNApol II, allowing it to backtrack and expose the lesion site to NER factors. TFIIS stimulates RNA cleavage by RNApol II during this process. NER factors unwinds DNA around the lesion. While RPA protects ssDNA from degradation, XPG and XPF-ERCC1 endonucleases cleave the strand containing the lesion. DNA polymerase and ligase then fill up the gap. CSB degradation is necessary to RNA synthesis recovery.

Figure 1