Mouse Anti-ERCC3 Recombinant Antibody (EG1131) (CBMAB-EN1348-LY)

Name: Mouse Anti-ERCC3 Recombinant Antibody (EG1131)
SKU: CBMAB-EN1348-LY
Rating: 5 (1 reviews)

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Published Data

Mouse Anti-ERCC3 Recombinant Antibody (EG1131) (CBMAB-EN1348-LY) in WB

Representative gel and protein levels of XPA, XPB, XPC, XPF, DDB1, XPD, XPG, and DDB2 in VEH- and EDC-MMSCs isolated from 5-month-old rats. Data were normalized by the amount of β-actin protein levels. ...View More

Bariani, M. V., Cui, Y. H., Ali, M., Bai, T., Grimm, S. L., Coarfa, C., ... & Al-Hendy, A. (2023). TGFβ signaling links early life endocrine-disrupting chemicals exposure to suppression of nucleotide excision repair in rat myometrial stem cells. Cellular and Molecular Life Sciences, 80(10), 288.

Mouse Anti-ERCC3 Recombinant Antibody (EG1131) (CBMAB-EN1348-LY) in WB

The different expression levels of WSTF, XPB, and RPB1 is shown. ...View More

Kang, D., Liu, Y., Song, Y., Fang, B., Zhang, Q., & Hu, L. (2022). Triptolide shows high sensitivity and low toxicity against acute myeloid leukemia cell lines through inhibiting WSTF-RNAPII complex. Frontiers in Oncology, 12, 811850.

Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

EG1131

Application

IP, WB

Immunogen

Recombinant fragment of human ERCC3 (C-terminus).

Host Species

Mouse

Specificity

Human, Mouse, Rat, Monkey

Antibody Isotype

IgG2a

Clonality

Monoclonal Antibody

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
WB	1:1,000
IP	1:50

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

Format

Liquid

Buffer

HEPES, BSA, glycerol

Preservative

Sodium azide

Concentration

Batch dependent

Purity

> 95% Purity determined by SDS-PAGE.

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

More Infomation

Target

Full Name

ERCC Excision Repair 3, TFIIH Core Complex Helicase Subunit

Introduction

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. [provided by RefSeq, Dec 2014]

Entrez Gene ID

Human	2071
Mouse	13872
Rat	291703

UniProt ID

Human	P19447
Mouse	P49135
Rat	Q4G005

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.

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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

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