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Human Polyclonal NHEJ1 Primary Antibody for WB - ABIN658424
Malivert, Ropars, Nunez, Drevet, Miron, Faure, Guerois, Mornon, Revy, Charbonnier, Callebaut, de Villartay: Delineation of the Xrcc4-interacting region in the globular head domain of cernunnos/XLF. in The Journal of biological chemistry 2010
Show all 3 references for ABIN658424
Human Polyclonal NHEJ1 Primary Antibody for IHC, ELISA - ABIN185719
Ahnesorg, Smith, Jackson: XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining. in Cell 2006
Human Polyclonal NHEJ1 Primary Antibody for IP, WB - ABIN223427
Liu, Liu, Kamdar, Wanotayan, Sharma, Adachi, Matsumoto: C-Terminal region of DNA ligase IV drives XRCC4/DNA ligase IV complex to chromatin. in Biochemical and biophysical research communications 2013
using dual- and quadruple-trap optical tweezers combined with fluorescence microscopy, we show how human XRCC4 (show XRCC4 Antibodies), XLF and XRCC4 (show XRCC4 Antibodies)-XLF complexes interact with DNA in real time
The data suggest that XLF has multiple functions in DNA repair, and they offer potential explanations for the pleiotropic phenotypes associated with XLF deficiency.
PC4 (show IFRD1 Antibodies) protects esophageal squamous cell carcinoma cells from IR-induced death by enhancing the nonhomologous end joining-promoting activity of XLF.
Phosphorylation of XLF impairs non-homologous end-joining DNA repair.
Werner syndrome protein positively regulates XRCC4-like factor transcription.
Human XLF is a non-essential, but critical, classic non-homologous end-joining -repair factor.
An induced pluripotent stem cell (iPSC) model of XLF deficiency, which accurately replicates the double-strand break repair deficiency observed in XLF syndrome patients, is reported.
Data indicate that Ku70 (show XRCC6 Antibodies)/Ku80 (show XRCC5 Antibodies) facilitates the cooperative binding of multiple XRCC4 (show XRCC4 Antibodies)/Ligase IV (XL) and XLF molecules to DNA.
XRCC4 (show XRCC4 Antibodies) and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair. (Review)
Cernunnos deficiency results in chronic activation of the DNA damage response, P53 (show TP53 Antibodies)-driven upregulation of proapoptotic factors, leading to decreased thymocyte viability and a qualitative alteration of the T cell repertoire in both humans and mice.
These results reveal an unanticipated functional interplay between the RAG complex and XLF in repairing RAG-induced DNA breaks and maintaining genome integrity during antigen receptor gene assembly.
XLF-deficient mice recapitulate the age-dependent lymphocytopenia of patients.
XLF functionally overlaps with DNA-PKcs in normal development, promotion of genomic stability in fibroblasts, and in IgH class switch recombination in mature B cells.
XLF repair protein and 53BP1 (show TP53BP1 Antibodies) DNA damage response factor have overlapping functions in end joining and lymphocyte development
find that combined XLF/53BP1 (show TP53BP1 Antibodies) deficiency in mice severely impairs C-NHEJ, V(D)J recombination, and lymphocyte development while also leading to general genomic instability and growth defects
XLF, ATM and H2AX all have fundamental roles in processing and joining DNA ends during V(D)J recombination, but that these roles have been masked by unanticipated functional redundancies
in mice, Cernunnos-XLF is essential for normal NHEJ-mediated repair of DNA DSBs and the Cernunnos-XLF acts as a genomic caretaker to prevent genomic instability
Double-strand breaks in DNA result from genotoxic stresses and are among the most damaging of DNA lesions. This gene encodes a DNA repair factor essential for the nonhomologous end-joining pathway, which preferentially mediates repair of double-stranded breaks. Mutations in this gene cause different kinds of severe combined immunodeficiency disorders.
nonhomologous end-joining factor 1
, non-homologous end-joining factor 1
, XRCC4-like factor
, protein cernunnos