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ProteomicsPAXX is an accessory c-NHEJ factor that associates with Ku70 and has overlapping functions with XLF
In mammalian cells, classical non-homologous end joining (c-NHEJ) is critical for DNA double-strand break repair induced by ionizing radiation and during V(D)J recombination in developing B and T lymphocytes. Recently, PAXX was identified as a new c-NHEJ core component. We report here, that PAXX-def...
ORGANISM(S): Homo sapiens (Human) 
2016-10-06 | PXD004659 | Pride
Non-homologous end joining Micro-homology mediated end joining V(d)j recombination Genomic instability Dna double-strand break 
GenomicsTargeted MIP sequencing for healthy samples
We developed Del-Read, an algorithm targeting medium-sized deletions (6-100 BPs) in short-reads, which are challenging for current variant callers relying on alignment. Our focus was on Micro-Homology mediated End Joining deletions (MMEJ-dels), prevalent in myeloid malignancies. MMEJ-dels follow a d...
ORGANISM(S): Homo sapiens 
2023-09-20 | E-MTAB-13306 | biostudies-arrayexpress
UnknownPoly ADP Ribose Polymerase Inhibitor Olaparib Targeting Microhomology End Joining in Retinoblastoma Protein Defective Cancer: Analysis of the Retinoblastoma Cell-Killing Effects by Olaparib after Inducing Double-Strand Breaks.
Not available
S-EPMC8508856 | biostudies-literature
UnknownRB Regulates DNA Double Strand Break Repair Pathway Choice by Mediating CtIP Dependent End Resection.
Not available
S-EPMC7730402 | biostudies-literature
UnknownEEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair.
Not available
S-EPMC4684289 | biostudies-literature
UnknownSingle AAV-mediated mutation replacement genome editing in limited number of photoreceptors restores vision in mice.
Not available
S-EPMC6981188 | biostudies-literature
GenomicsCopy number variations (CNVs) are a form of genetic alteration strongly implicated in numerous neurological and psychiatric disorders, as well as brain cancer. Replication stress is a common cause of CNVs. Despite the prevailing model that CNVs arise from DNA double strand breaks (DSBs), there has been no assay that directly perturbs presumed DSB sources and measures CNV output. Here, we identified a subset of recurrent DNA break clusters (RDCs) as a causal factor for CNV formation. In murine neural progenitor cells under replication stress, mapping the formation of CNVs revealed their location in RDC regions that contain actively transcribed genes. Single-cell structural variant mapping in the subsequent cell cycle revealed a significant breakpoint correlation with RDCs. CRISPR/Cas9-mediated transcriptional suppression abrogated both RDC and CNV formation, but does not alter their replication timing. We found that DNA polymerase theta (Pol θ), a protector against CNV formation, plays ...
RDC-mediated genome diversification
PRJEB105360 | ENA
UnknownUnderstanding the diversity of genetic outcomes from CRISPR-Cas generated homology-directed repair.
Not available
S-EPMC6898364 | biostudies-literature
UnknownZebrafish Polymerase Theta and human Polymerase Theta: Orthologues with homologous function.
Not available
S-EPMC12040184 | biostudies-literature
UnknownZebrafish Polymerase Theta and human Polymerase Theta: orthologues with homologous function.
Not available
S-EPMC11463350 | biostudies-literature
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