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Human Polyclonal NHEJ1 Primary Antibody for IHC (p), IHC - ABIN251685
Ahnesorg, Smith, Jackson: XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining. in Cell 2006
Show all 2 Pubmed References
Human Monoclonal NHEJ1 Primary Antibody for FACS, ICC - ABIN4366409
Reid, Keegan, Leo-Macias, Watanabe, Strande, Chang, Oksuz, Fenyo, Lieber, Ramsden, Rothenberg: Organization and dynamics of the nonhomologous end-joining machinery during DNA double-strand break repair. in Proceedings of the National Academy of Sciences of the United States of America 2015
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
TDP1 (show TDP1 Antibodies) participation in human non-homologous end joining (NHEJ) is mediated by interaction with XLF, and that TDP1 (show TDP1 Antibodies)-XLF interactions and subsequent NHEJ events are regulated by phosphorylation of TDP1 (show TDP1 Antibodies)-S81.
The role of XLF in NHEJ is summarized.
XLF has an important role during V(D)J recombination.
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.
Ku70 is epistatic with XLF and DNA-PKcs and support a model in which inactivation of Ku70 allows DNA lesions to become accessible to alternative DNA repair pathways (other than Classical Non-Homologous End-Joining (C-NHEJ)).
PAXX and XLF proteins may have redundant functions during Non-homologous end joining.
Paxx/Xlf double-knockout mice display embryonic lethality associated with genomic instability, cell death in the central nervous system, and an almost complete block in lymphogenesis
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.
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.
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
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