XPB and XPD are ATPase/helicase subunits of the TFIIH complex that are involved in nucleotide excision repair (NER) to remove lesions and photoproducts generated by UV light. XPB and XPD are 3’-5’ and 5’-3’ DNA helicases, respectively, that play a role in opening of the DNA damage site to facilitate repair. XPB and XPD both play an important role in maintaining genomic stability, and researchers have linked mutations of these proteins to Xeroderma Pigmentosum (XP) and Trichothiodystrophy (TTD). XP patients have abnormalities in skin pigmentation and are highly susceptible to skin cancers, while TTD patients exhibit symptoms such as brittle hair, neurological abnormalities, and mild photosensitivity. In addition to their role in NER, XPB and XPD are involved in transcription initiation as part of the TFIIH core complex. The helicase activity of XPB unwinds DNA around the transcription start site to facilitate RNA polymerase II promoter clearance and initiation of transcription. XPD plays a structural role linking core TFIIH components with the cdk-activating kinase (CAK) complex that phosphorylates the C-terminus of the largest subunit of RNA polymerase II, leading to transcription initiation.
XPB and XPD are ATPase/helicase subunits of the TFIIH complex that are involved in nucleotide excision repair (NER) to remove lesions and photoproducts generated by UV light. XPB and XPD are 3’-5’ and 5’-3’ DNA helicases, respectively, that play a role in opening of the DNA damage site to facilitate repair. XPB and XPD both play an important role in maintaining genomic stability, and researchers have linked mutations of these proteins to Xeroderma Pigmentosum (XP) and Trichothiodystrophy (TTD). XP patients have abnormalities in skin pigmentation and are highly susceptible to skin cancers, while TTD patients exhibit symptoms such as brittle hair, neurological abnormalities, and mild photosensitivity. In addition to their role in NER, XPB and XPD are involved in transcription initiation as part of the TFIIH core complex. The helicase activity of XPB unwinds DNA around the transcription start site to facilitate RNA polymerase II promoter clearance and initiation of transcription. XPD plays a structural role linking core TFIIH components with the cdk-activating kinase (CAK) complex that phosphorylates the C-terminus of the largest subunit of RNA polymerase II, leading to transcription initiation.
ERCC3 is an ATP-dependent DNA helicase that functions in nucleotide excision repair and complements xeroderma pigmentosum group B mutations. It also is the 89 kDa subunit of basal transcription factor 2 (TFIIH) and thus functions in class II transcription.
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.
Pathway
DNA repair pathway
Protein Families
Helicase family, RAD25/XPB subfamily
Buffer
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Format
liquid
Purification
Affinity purification
Purity
Affinity purification
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Storage Buffer
Store at -20oC or -80oC. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.