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Phospho-blocking and -mimicking mutations impact both the stability and DNA bridging capacity of XRCC4 (show XRCC4 Proteins)/XLF complexes, but without affecting their ability to stimulate LIG4 (show LIG4 Proteins) activity. Implicit in this finding is that phosphorylation may regulate DNA bridging by XRCC4 (show XRCC4 Proteins)/XLF filaments.
Chemotherapy-induced overexpression of XLF and XLF-mediated enhancements in NHEJ activity contribute to chemoresistance in hepatocellular carcinoma (HCC (show FAM126A Proteins)) cells and patients with HCC (show FAM126A Proteins). Targeting XLF to modulate DSB repair could enhance drug sensitivity and may be a therapeutically useful addition to conventional therapy
TDP1 (show TDP1 Proteins) participation in human non-homologous end joining (NHEJ) is mediated by interaction with XLF, and that TDP1 (show TDP1 Proteins)-XLF interactions and subsequent NHEJ events are regulated by phosphorylation of TDP1 (show TDP1 Proteins)-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 Proteins), XLF and XRCC4 (show XRCC4 Proteins)-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 Proteins) 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.
we also find that PAXX deficiency has no impact on V(D)J recombination DSB joining in ATM (show ATM Proteins)-deficient pro-B lines. We discuss implications of these findings with respect to potential PAXX and XLF functions in C-NHEJ.
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 Proteins)-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 Proteins) DNA damage response factor have overlapping functions in end joining and lymphocyte development
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