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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: DNA Repair (Amst). 2021 Apr 20;103:103126. doi: 10.1016/j.dnarep.2021.103126

Figure 1.

Figure 1.

TC-NER in mammalian cells. RNA Pol II stalling at a DNA lesion leads to the binding of CSB, which recruits CSA and UVSSA. UVSSA then promotes TFIIH recruitment. The elongation factor ELOF1 and the serine/threonine kinase STK19 are also important for TC-NER, but their roles remain elusive. The helicases in TFIIH unwind the two strands of damaged DNA to facilitate dual incision by ERCC1-XPF and XPG on the 5’ and 3’ sides of the lesion, respectively. The excised DNA fragment containing the lesion is bound by TFIIH and released. The gap on the damaged strand is filled by DNA polymerases and DNA ligases. Transcription can be resumed after repair of the damage.