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Mouse Anti-ERCC3 Recombinant Antibody (CBYJT-1237) (CBMAB-T0252-YJ)


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Summary

Host Animal
Mouse
Specificity
Human, Rat, Mouse
Clone
CBYJT-1237
Antibody Isotype
IgG
Application
WB, IP, IF, ELISA

Basic Information

Immunogen
Amino acids 483-782 mapping at the C-terminus of TFIIH p89 of human origin
Specificity
Human, Rat, Mouse
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
PBS, pH 7.4
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 483-782

Target

Full Name
ERCC Excision Repair 3, TFIIH Core Complex Helicase Subunit
Introduction
ERCC3 is an ATP-dependent DNA helicase that functions in nucleotide excision repair. ERCC3 is a subunit of basal transcription factor 2 (TFIIH) and, therefore, also functions in class II transcription. Mutations in ERCC3 are associated with Xeroderma pigmentosum B, Cockayne's syndrome, and trichothiodystrophy.
Entrez Gene ID
Human2071
Mouse13872
Rat291703
UniProt ID
HumanP19447
MouseP49135
RatQ4G005
Alternative Names
ERCC Excision Repair 3, TFIIH Core Complex Helicase Subunit; Excision Repair Cross-Complementing Rodent Repair Deficiency, Complementation Group 3; TFIIH Basal Transcription Factor Complex 89 KDa Subunit; Xeroderma Pigmentosum Group B-Complementing Protein; Excision Repair Cross-Complementation Group 3; Basic Transcription Factor 2 89 KDa Subunit; DNA Repair Protein Complementing XP-B Cells; DNA Excision Repair Protein ERCC-3; TFIIH 89 KDa Subunit; TFIIH P89; BTF2 P89; XPB; TFIIH Basal Transcription Factor Complex Helicase XPB Subunit
Research Area
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 (PubMed:8157004, PubMed:30894545).

When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape (PubMed:8157004).

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.
Biological Process
Apoptotic process Source: UniProtKB
DNA repair Source: UniProtKB
DNA topological change Source: UniProtKB
Embryonic organ development Source: GO_Central
Hair cell differentiation Source: UniProtKB
Nucleotide-excision repair Source: UniProtKB
Nucleotide-excision repair, DNA duplex unwinding Source: UniProtKB
Nucleotide-excision repair, DNA incision Source: UniProtKB
Positive regulation of apoptotic process Source: UniProtKB
Protein localization Source: UniProtKB
Regulation of mitotic cell cycle phase transition Source: UniProtKB
Response to hypoxia Source: Ensembl
Response to oxidative stress Source: UniProtKB
Response to UV Source: UniProtKB
Transcription by RNA polymerase II Source: UniProtKB
Transcription-coupled nucleotide-excision repair Source: UniProtKB
Transcription elongation from RNA polymerase II promoter Source: Reactome
Transcription elongation from RNA polymerase I promoter Source: Ensembl
Transcription initiation from RNA polymerase II promoter Source: GO_Central
UV protection Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
Xeroderma pigmentosum complementation group B (XP-B):
An autosomal recessive pigmentary skin disorder characterized by solar hypersensitivity of the skin, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. The skin develops marked freckling and other pigmentation abnormalities. Some XP-B patients present features of Cockayne syndrome, including cachectic dwarfism, pigmentary retinopathy, ataxia, decreased nerve conduction velocities. The phenotype combining xeroderma pigmentosum and Cockayne syndrome traits is referred to as XP-CS complex.
Trichothiodystrophy 2, photosensitive (TTD2):
A form of trichothiodystrophy, an autosomal recessive disease characterized by sulfur-deficient brittle hair and multisystem variable abnormalities. The spectrum of clinical features varies from mild disease with only hair involvement to severe disease with cutaneous, neurologic and profound developmental defects. Ichthyosis, intellectual and developmental disabilities, decreased fertility, abnormal characteristics at birth, ocular abnormalities, short stature, and infections are common manifestations. There are both photosensitive and non-photosensitive forms of the disorder.
More Infomation

Stradella, A., Del Valle, J., Brunet, J., & Lázaro, C. (2021). Response to letter entitled: Re: ERCC3 a new ovarian cancer susceptibility gene?. European journal of cancer (Oxford, England: 1990), 150, 281-282.

Soukupova, J., Zemankova, P., Nehasil, P., Kleibl, Z., Kleibl, Z., Soukupová, J., ... & Macůrek, L. (2021). Re: ERCC3, a new ovarian cancer susceptibility gene?. European Journal of Cancer, 150, 278-280.

Wang, S., Liu, W., Ni, Y., Wang, L., Zhu, Y., Shi, Q., ... & Yang, Z. (2021). Overexpression of ERCC3 is associated with poor prognosis in patients with pancreatic cancer. Journal of Cancer, 12(9), 2550.

Mok, E. H. K., Leung, C. O. N., & Lee, T. K. W. (2020). MAP9/ERCC3 signaling cascade: A new insight on understanding the chromosomal instability in hepatocellular carcinoma. EBioMedicine, 54.

Stradella, A., Del Valle, J., Rofes, P., Vargas-Parra, G., Salinas, M., González, S., ... & Lázaro, C. (2020). ERCC3, a new ovarian cancer susceptibility gene?. European Journal of Cancer, 141, 1-8.

Zhang, J., Huang, J. Z., Zhang, Y. Q., Zhang, X., Zhao, L. Y., Li, C. G., ... & Yu, J. (2020). Microtubule associated protein 9 inhibits liver tumorigenesis by suppressing ERCC3. EBioMedicine, 53, 102701.

Xie, X., Huang, N., Zhang, Y., Wei, X., Gao, M., Li, M., ... & Gu, K. (2019). MiR-192-5p reverses cisplatin resistance by targeting ERCC3 and ERCC4 in SGC7901/DDP cells. Journal of Cancer, 10(4), 1039.

Li, M., Gao, M., Xie, X., Zhang, Y., Ning, J., Liu, P., & Gu, K. (2019). MicroRNA‑200c reverses drug resistance of human gastric cancer cells by targeting regulation of the NER‑ERCC3/4 pathway. Oncology Letters, 18(1), 145-152.

Topka, S., Khalil, S., Stanchina, E. D., Vijai, J., & Offit, K. (2018). Preclinical evaluation of enhanced irofulven antitumor activity in an ERCC3 mutant background by in vitro and in vivo tumor models. Cancer Research, 78(13_Supplement), 3258-3258.

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For research use only. Not intended for any clinical use.

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