Anti-XPB/ERCC3 Antibody Picoband® Fluoro488 Conjugated

XPB (xeroderma pigmentosum type B) is an ATP-dependent DNA helicase in humans that is a part of the TFIIH transcription factor complex. This gene encodes an ATP-dependent DNA helicase that functions in nucleotide excision repair. The encoded protein is a subunit of basal transcription factor 2 (TFIIH) and, therefore, also functions in class II transcription. Mutations in this gene are associated with Xeroderma pigmentosum B, Cockayne's syndrome, and trichothiodystrophy. Alternative splicing results in multiple transcript variants.

General transcription and DNA repair factor IIH helicase subunit XPB; TFIIH subunit XPB; Basic transcription factor 2 89 kDa subunit; BTF2 p89; DNA excision repair protein ERCC-3; DNA repair protein complementing XP-B cells; TFIIH basal transcription factor complex 89 kDa subunit; TFIIH 89 kDa subunit; TFIIH p89; Xeroderma pigmentosum group B-complementing protein; ERCC3; XPB; XPBC

Mainly expressed in pachytene spermatocytes of testis and in lymphocyte-rich areas of spleen and lymph nodes. Isoform v1 is expressed in spleen. Isoform v2 is expressed in testis. Also detected in ovary, placenta, pancreas, cardiac fibroblasts. Expressed in B-cells and prostate malignant cells. Isoform v1 and isoform v3 are expressed in epithelial colorectal adenocarcinoma cells. Isoform v2 and isoform v4 are expressed in endothelial cells. Isoform v1, isoform v2, isoform v3 and isoform v4 are expressed in pulmonary artery smooth muscle cells. Isoform v2 and isoform v5 are expressed in microvascular endothelial cells (at protein level) .

Cancer, Cancer Metabolism, DNA/RNA, DNA Damage & Repair, Epigenetics and Nuclear Signaling, Metabolic Signaling Pathways, Metabolism, Metabolism Processes, Nucleotide Metabolism, Pathways and Processes, Response To Hypoxia

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.

1. Coin, F., Oksenych, V., Egly, J.-M. Distinct roles for the XPB/p52 and XPD/p44 subcomplexes of TFIIH in damaged DNA opening during nucleotide excision repair. Molec. Cell 26: 245-256, 2007. 2. Kim, T.-K., Ebright, R. H., Reinberg, D. Mechanism of ATP-dependent promoter melting by transcription factor IIH. Science 288: 1418-1421, 2000. 3. Le May, N., Dubaele, S., De Santis, L. P., Billecocq, A., Bouloy, M., Egly, J.-M.TFIIH transcription factor, a target for the Rift Valley hemorrhagic fever virus. Cell 116: 541-550, 2004.