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Mouse Anti-ERCC4 Recombinant Antibody (UMAB20) (CBMAB-X0031-YC)


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Summary

Host Animal
Mouse
Specificity
Human, Dog, Rat, Monkey, Mouse
Clone
UMAB20
Antibody Isotype
IgG2a
Application
WB, IF, FC, IHC

Basic Information

Immunogen
Full length recombinant protein of human XPF (NP_005227) produced in HEK293 cell.
Specificity
Human, Dog, Rat, Monkey, Mouse
Antibody Isotype
IgG2a
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!]

Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
ERCC Excision Repair 4, Endonuclease Catalytic Subunit
Introduction
ERCC4 is catalytic component of a structure-specific DNA repair endonuclease responsible for the 5-prime incision during DNA repair, which is a structure specific DNA repair endonuclease that interacts with EME1. ERCC4 is involved in homologous recombination that assists in removing interstrand cross-link. Defects in ERCC4 are a cause of xeroderma pigmentosum complementation group F (XP-F), or xeroderma pigmentosum VI (XP6).
Entrez Gene ID
Human2072
Mouse50505
Rat304719
Monkey712641
Dog479842
UniProt ID
HumanQ92889
MouseQ9QZD4
RatD3ZT95
MonkeyA0A0D9R727
DogE2QYD6
Alternative Names
XPF; RAD1; FANCQ; XFEPS; ERCC11
Research Area
Catalytic component of a structure-specific DNA repair endonuclease responsible for the 5-prime incision during DNA repair. Involved in homologous recombination that assists in removing interstrand cross-link.
Biological Process
Cellular response to UV Source: BHF-UCL
DNA repair Source: UniProtKB
Double-strand break repair via homologous recombination Source: UniProtKB
Double-strand break repair via nonhomologous end joining Source: BHF-UCL
Negative regulation of double-stranded telomeric DNA binding Source: BHF-UCL
Negative regulation of protection from non-homologous end joining at telomere Source: BHF-UCL
Negative regulation of telomerase activity Source: GOC
Negative regulation of telomere maintenance Source: UniProtKB
Negative regulation of telomere maintenance via telomere lengthening Source: BHF-UCL
Nucleotide-excision repair Source: MGI
Nucleotide-excision repair, DNA incision Source: UniProtKB
Nucleotide-excision repair, DNA incision, 3'-to lesion Source: UniProtKB
Nucleotide-excision repair, DNA incision, 5'-to lesion Source: UniProtKB
Nucleotide-excision repair involved in interstrand cross-link repair Source: GO_Central
Regulation of autophagy Source: Ensembl
Resolution of meiotic recombination intermediates Source: GO_Central
Response to UV Source: UniProtKB
Telomere maintenance Source: BHF-UCL
Telomeric DNA-containing double minutes formation Source: BHF-UCL
UV protection Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
Xeroderma pigmentosum complementation group F (XP-F):
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. XP-F patients show a mild phenotype.
XFE progeroid syndrome (XFEPS):
A syndrome characterized by aged bird-like facies, lack of subcutaneous fat, dwarfism, cachexia and microcephaly. Additional features include sun-sensitivity from birth, learning disabilities, hearing loss, and visual impairment.
Xeroderma pigmentosum type F/Cockayne syndrome (XPF/CS):
A variant form of Cockayne syndrome, a disorder characterized by growth retardation, microcephaly, impairment of nervous system development, pigmentary retinopathy, peculiar facies, and progeria together with abnormal skin photosensitivity. Cockayne syndrome dermatological features are milder than those in xeroderma pigmentosum and skin cancers are not found in affected individuals. XPF/CS patients, however, present with severe skin phenotypes, including severe photosensitivity, abnormal skin pigmentation, and skin cancer predisposition.
Fanconi anemia complementation group Q (FANCQ):
A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.
More Infomation

Sahaba, S. A., Rashid, M. A., Islam, M., Nahid, N. A., Apu, M. N. H., Sultana, T. N., ... & Islam, M. S. (2022). The link of ERCC2 rs13181 and ERCC4 rs2276466 polymorphisms with breast cancer in the Bangladeshi population. Molecular Biology Reports, 49(3), 1847-1856.

Wu, J. J., Jin, J., Li, Y. H., Wang, C., Bai, J., Jiang, Q. J., ... & Qu, L. F. (2022). LncRNA FGF7-5 and lncRNA GLRX3 together inhibits the formation of carotid plaque via regulating the miR-2681-5p/ERCC4 axis in atherosclerosis. Cell Cycle, 1-18.

Anjali, K., Kumar, T., Kumar, P., Narayan, G., & Singh, S. (2022). Association of nonsynonymous SNPs of nucleotide excision repair genes ERCC4 rs1800067 (G/A) and ERCC5 rs17655 (G/C) as predisposing risk factors for gallbladder cancer. Digestive and Liver Disease.

Sreekumar, R., Al‐Saihati, H., Emaduddin, M., Moutasim, K., Mellone, M., Patel, A., ... & Sayan, A. E. (2021). The ZEB2‐dependent EMT transcriptional programme drives therapy resistance by activating nucleotide excision repair genes ERCC1 and ERCC4 in colorectal cancer. Molecular Oncology, 15(8), 2065-2083.

Das, S., Naher, L., Aka, T. D., Aziz, M. A., Shabnaz, S., Shahriar, M., & Islam, M. S. (2021). The ECCR1 rs11615, ERCC4 rs2276466, XPC rs2228000 and XPC rs2228001 polymorphisms increase the cervical cancer risk and aggressiveness in the Bangladeshi population. Heliyon, 7(1), e05919.

Hu, H., Liu, S., Chu, A., Chen, J., Xing, C., & Jing, J. (2021). Comprehensive analysis of ceRNA network of ERCC4 in colorectal cancer. PeerJ, 9, e12647.

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.

Ning, J., Jiao, Y., Xie, X., Deng, X., Zhang, Y., Yang, Y., ... & Gu, K. (2019). miR‑138‑5p modulates the expression of excision repair cross‑complementing proteins ERCC1 and ERCC4, and regulates the sensitivity of gastric cancer cells to cisplatin. Oncology Reports, 41(2), 1131-1139.

Guiraldelli, M. F., Felberg, A., Almeida, L. P., Parikh, A., de Castro, R. O., & Pezza, R. J. (2018). SHOC1 is a ERCC4-(HhH) 2-like protein, integral to the formation of crossover recombination intermediates during mammalian meiosis. PLoS genetics, 14(5), e1007381.

Tezuka, S., Ueno, M., Kobayashi, S., Morimoto, M., Ohkawa, S., Hirotani, A., ... & Maeda, S. (2018). Predictive value of ERCC1, ERCC2, ERCC4, and glutathione S-Transferase Pi expression for the efficacy and safety of FOLFIRINOX in patients with unresectable pancreatic cancer. American Journal of Cancer Research, 8(10), 2096.

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

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