Human XRCC4 ELISA Matched Antibody Pair

Name: Human XRCC4 ELISA Matched Antibody Pair
SKU: ABPR-1037
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Species Reactivity

Human

Intended Use

This antibody pair set comes with matched antibody pair to detect and quantify protein level of human XRCC4.

General Description

The protein encoded by this gene functions together with DNA ligase IV and the DNA-dependent protein kinase in the repair of DNA double-strand break by non-homologous end joining and the completion of V(D)J recombination events. The non-homologous end-joining pathway is required both for normal development and for suppression of tumors. This gene functionally complements XR-1 Chinese hamster ovary cell mutant, which is impaired in DNA double-strand breaks produced by ionizing radiation and restriction enzymes. Alternative transcription initiation and alternative splicing generates several transcript variants.

Reconstitution And Storage

Store reagents of the antibody pair set at -20°C or lower. Please aliquot to avoid repeated freeze thaw cycle. Reagents should be returned to -20°C storage immediately after use.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination

CELL REPORTS

Authors: Lescale, Chloe; Hasse, Helene Lenden; Blackford, Andrew N.; Balmus, Gabriel; Bianchi, Joy J.; Yu, Wei; Bacoccina, Lea; Jarade, Angelique; Clouin, Christophe; Sivapalan, Rohan; Reina-San-Martin, Bernardo; Jackson, Stephen P.; Deriano, Ludovic

Abstract

Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V(D)J recombination are masked by redundant joining activities. Thus, combined PAXX and XLF deficiency leads to an inability to join RAG-cleaved DNA ends. Additionally, we demonstrate that PAXX function in V(D)J recombination depends on its interaction with Ku. Importantly, we show that, unlike XLF, the role of PAXX during the repair of DNA breaks does not overlap with ATM and the RAG complex. Our findings illuminate the role of PAXX in V(D)J recombination and support a model in which PAXX and XLF function during NHEJ repair of DNA breaks, whereas XLF, the RAG complex, and the ATM-dependent DNA damage response promote end joining by stabilizing DNA ends.

eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia

BRATISLAVA MEDICAL JOURNAL-BRATISLAVSKE LEKARSKE LISTY

Authors: Pehlivan, S.; Uysal, M. A.; Aydin, P. C.; Pehlivan, M.; Nursal, A. F.; Yavuzlar, H.; Kurnaz, S.; Sever, U.; Yavuz, F. K.; Uysal, S.; Aydin, N.

Abstract

BACKGROUND: This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (eNOS) and the XRCC4 gene play any role in nicotine dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis. METHODS: Present study included 100 individuals with ND, 60 patients with Sch+ND, and 70 healthy controls. These variants were analyzed using PCR. RESULTS: The cases with ND had higher eNOS VNTR-BB genotype than the healthy control subjects (p = 0.001). eNOS-AA genotype was lower in cases with Sch+ND and ND groups compared to the controls (p = 0.001, p = 0.001, respectively). eNOS-B allele was found significantly more frequently in Sch+ND group compared to the controls (p = 0.001). eNOS-A allele was significantly lower in ND group than the controls (p = 0.001). XRCC4-ID genotype was more common in the ND group than the control group (p = 0.001) as heterozygosity disadvantage. XRCC4-DD genotype was more common in the Sch+ND group compared to the controls (p = 0.035). The frequency of XRCC4-I allele was lower in the Sch+ND group compared to the controls (p = 0.012). CONCLUSIONS: Our results showed that eNOS and XRCC4 VNTR variants might play a potential role in Sch+ND and/or ND pathophysiology (Tab. 2, Ref. 48). Text in PDF www.elis.sk.