Results 1 to 10 of about 55,685 (156)

Structure and mechanism in non-homologous end joining. [PDF]

open access: yesDNA Repair (Amst), 2023
DNA double-stranded breaks (DSBs) are a particularly challenging form of DNA damage to repair because the damaged DNA must not only undergo the chemical reactions responsible for returning it to its original state, but, additionally, the two free ends can become physically separated in the nucleus and must be bridged prior to repair.
Vogt A, He Y.
europepmc   +3 more sources

Functional Radiogenetic Profiling Implicates ERCC6L2 in Non-homologous End Joining [PDF]

open access: yesCell Reports, 2020
Summary: Using genome-wide radiogenetic profiling, we functionally dissect vulnerabilities of cancer cells to ionizing radiation (IR). We identify ERCC6L2 as a major determinant of IR response, together with classical DNA damage response genes and ...
Paola Francica   +20 more
doaj   +5 more sources

Saccharomyces cerevisiae Rev7 promotes non-homologous end-joining by blocking Mre11 nuclease and Rad50’s ATPase activities and homologous recombination [PDF]

open access: yeseLife
Recent studies have shown that, in human cancer cells, the tetrameric Shieldin complex (comprising REV7, SHLD1, SHLD2, and SHLD3) facilitates non-homologous end-joining (NHEJ) while blocking homologous recombination (HR). Surprisingly, several eukaryotic
Sugith Badugu   +3 more
doaj   +2 more sources

A Mechanism to Minimize Errors during Non-homologous End Joining [PDF]

open access: yesMolecular Cell, 2020
Enzymatic processing of DNA underlies all DNA repair, yet inappropriate DNA processing must be avoided. In vertebrates, double-strand breaks are repaired predominantly by non-homologous end joining (NHEJ), which directly ligates DNA ends. NHEJ has the potential to be highly mutagenic because it uses DNA polymerases, nucleases, and other enzymes that ...
Johannes C Walter, Joseph J Loparo
exaly   +3 more sources

The role of RecQ helicases in non-homologous end-joining [PDF]

open access: yesCritical Reviews in Biochemistry and Molecular Biology, 2014
DNA double-strand breaks are highly toxic DNA lesions that cause genomic instability, if not efficiently repaired. RecQ helicases are a family of highly conserved proteins that maintain genomic stability through their important roles in several DNA repair pathways, including DNA double-strand break repair.
Guido Keijzers   +2 more
exaly   +4 more sources

Non-Homologous End-Joining Pathway Genotypes Significantly Associated with Nasopharyngeal Carcinoma Susceptibility [PDF]

open access: yesBiomedicines, 2023
Defects in the non-homologous end-joining (NHEJ) DNA repair pathway lead to genomic instability and carcinogenesis. However, the roles of individual NHEJ genes in nasopharyngeal carcinoma (NPC) etiology are not well-understood.
Chia-Wen Tsai   +8 more
doaj   +2 more sources

Mycobacterial non-homologous end joining is required for antiphage defense. [PDF]

open access: yesNucleic Acids Res
Abstract In the ongoing arms race with phages, bacteria have evolved diverse defense systems, such as CRISPR–Cas and restriction–modification systems. The DNA double-strand break repair system represents a core mechanism for maintaining genomic integrity and is vital for cell survival. However, it remains unknown whether and how these
Huang Y   +9 more
europepmc   +3 more sources

Non-homologous end joining: Emerging themes and unanswered questions [PDF]

open access: yesDNA Repair, 2014
Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation induced DNA double strand breaks in human cells. Here, we discuss current insights into the mechanism of NHEJ and the interplay between NHEJ and other pathways for repair of IR-induced DNA damage.
Sarvan Kumar Radhakrishnan   +1 more
exaly   +3 more sources

Up-Regulation of Non-Homologous End-Joining by MUC1 [PDF]

open access: yesGenes (Basel)
Ionizing radiation (IR) and chemotherapy with DNA-damaging drugs such as cisplatin are vital cancer treatment options. These treatments induce double-strand breaks (DSBs) as cytotoxic DNA damage; thus, the DSB repair activity in each cancer cell significantly influences the efficacy of the treatments.
europepmc   +3 more sources

Fusion of histone variants to Cas9 suppresses non-homologous end joining [PDF]

open access: yesPLoS ONE
Tomoko Kato-Inui   +3 more
doaj   +2 more sources

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