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The crystal structures of the Ku-binding motifs (KBM) of the non-homologous end joining (NHEJ) proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex are discussed.
PC4 expression correlated with radiosensitivity and was an independent prognostic factor of progression-free survival (PFS) in patients with NSCLC.
Synthetic lethality between DNA repair factors Xlf and Paxx is rescued by inactivation of Trp53
PAXX, XLF and XRCC4 synergise in the efficient DNA double-strand breaks recruitment, substrate recognition and stimulation of Pol lambda enzymatic activity during nonhomologous end joining DNA repair.
this study shows loss of NHEJ1 protein due to a novel splice site mutation in a family presenting with combined immunodeficiency, microcephaly, and growth retardation
Phospho-blocking and -mimicking mutations impact both the stability and DNA bridging capacity of XRCC4/XLF complexes, but without affecting their ability to stimulate LIG4 activity. Implicit in this finding is that phosphorylation may regulate DNA bridging by XRCC4/XLF filaments.
Chemotherapy-induced overexpression of XLF and XLF-mediated enhancements in NHEJ activity contribute to chemoresistance in hepatocellular carcinoma (HCC) cells and patients with HCC. Targeting XLF to modulate DSB repair could enhance drug sensitivity and may be a therapeutically useful addition to conventional therapy
TDP1 participation in human non-homologous end joining (NHEJ) is mediated by interaction with XLF, and that TDP1-XLF interactions and subsequent NHEJ events are regulated by phosphorylation of TDP1-S81.
Although PAXX-deficient cells lack c-NHEJ phenotypes, PAXX forms a stable ternary complex with Ku bound to DNA. Thus, PAXX plays an accessory role during c-NHEJ that is largely overlapped by XLF's function.
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, XLF and XRCC4-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 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/Ku80 facilitates the cooperative binding of multiple XRCC4/Ligase IV (XL) and XLF molecules to DNA.
XRCC4 and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair. (Review)
This damaging phenotype highlights the functional nexus between Xlf and Xrcc4, which is critical for the completion of NHEJ-dependent mechanisms during mouse development.
End joining of chromosomal breaks that are joined without causing insertion/deletion mutations requires several core canonical non-homologous end joining factors, including XLF. One of two binding domains of XLF is essential (L115 or C-terminal lysines that bind XRCC4 and KU/DNA, respectively), and that disruption of one of these domains sensitizes XLF to mutations that affect its dimer interface.
we also find that PAXX deficiency has no impact on V(D)J recombination DSB joining in ATM-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-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 DNA damage response factor have overlapping functions in end joining and lymphocyte development
find that combined XLF/53BP1 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