ATP-dependent 3'-5' DNA helicase, component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. The ATPase activity of XPB/ERCC3, but not its helicase activity, is required for DNA opening. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. The ATP-dependent helicase activity of XPB/ERCC3 is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. Belongs to the helicase family. RAD25/XPB subfamily. Note: This description may include information from UniProtKB.
Protein type: DNA repair, damage; EC 220.127.116.11; Helicase; Transcription factor
Molecular Function: 3'-5' DNA helicase activity; ATP binding; ATPase activity; damaged DNA binding; DNA binding; helicase activity; protein binding; protein C-terminus binding; protein N-terminus binding; transcription factor binding
Biological Process: 7-methylguanosine mRNA capping; apoptotic process; DNA repair; DNA topological change; global genome nucleotide-excision repair; hair cell differentiation; nucleotide-excision repair; nucleotide-excision repair, DNA duplex unwinding; nucleotide-excision repair, DNA incision; nucleotide-excision repair, DNA incision, 3'-to lesion; nucleotide-excision repair, DNA incision, 5'-to lesion; nucleotide-excision repair, preincision complex assembly; nucleotide-excision repair, preincision complex stabilization; positive regulation of apoptotic process; positive regulation of transcription by RNA polymerase II; protein localization; protein phosphorylation; regulation of mitotic cell cycle phase transition; response to hypoxia; response to oxidative stress; response to UV; termination of RNA polymerase I transcription; transcription by RNA polymerase II; transcription elongation from RNA polymerase I promoter; transcription elongation from RNA polymerase II promoter; transcription initiation from RNA polymerase I promoter; transcription initiation from RNA polymerase II promoter; transcription-coupled nucleotide-excision repair; UV protection; viral process