Results 21 to 30 of about 341,882 (288)

Non-homologous end joining: advances and frontiers [PDF]

open access: yesActa Biochimica et Biophysica Sinica, 2016
DNA double-strand breaks (DSBs) are the most serious form of DNA damage. In human cells, non-homologous end joining (NHEJ) is the major pathway for the repair of DSBs. Different types of DSBs result in different subsets of NHEJ repair strategies. These variations in NHEJ repair strategies depend on numerous elements, such as the flexible recruitment of
Kai, Yang, Rong, Guo, Dongyi, Xu
openaire   +2 more sources

Is non-homologous end-joining really an inherently error-prone process? [PDF]

open access: yesPLoS Genetics, 2014
DNA double-strand breaks (DSBs) are harmful lesions leading to genomic instability or diversity. Non-homologous end-joining (NHEJ) is a prominent DSB repair pathway, which has long been considered to be error-prone.
Mireille Bétermier   +2 more
doaj   +1 more source

Non-homologous end-joining, a sticky affair [PDF]

open access: yesOncogene, 2007
Rejoining of broken chromosomes is crucial for cell survival and prevention of malignant transformation. Most mammalian cells rely primarily on the non-homologous end-joining pathway of DNA double-strand break (DSB) repair to accomplish this task. This review focuses both on the core non-homologous end-joining machinery, which consists of DNA-dependent
van Gent, Dik, van der Burg, Mirjam
openaire   +2 more sources

Protocol: A Multiplexed Reporter Assay to Study Effects of Chromatin Context on DNA Double-Strand Break Repair

open access: yesFrontiers in Genetics, 2022
DNA double-strand breaks (DSBs) can be repaired through various pathways. Understanding how these pathways are regulated is of great interest for cancer research and optimization of gene editing.
Ruben Schep   +5 more
doaj   +1 more source

XLF acts as a flexible connector during non-homologous end joining

open access: yeseLife, 2020
Non-homologous end joining (NHEJ) is the predominant pathway that repairs DNA double-strand breaks in vertebrates. During NHEJ DNA ends are held together by a multi-protein synaptic complex until they are ligated.
Sean M Carney   +6 more
doaj   +1 more source

The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity. [PDF]

open access: yes, 2018
53BP1 controls a specialized non-homologous end joining (NHEJ) pathway that is essential for adaptive immunity, yet oncogenic in BRCA1 mutant cancers.
Sven Rottenberg (135593)   +41 more
core   +2 more sources

UBQLN4 promotes non-homologous end joining by repressing DNA end-resection

open access: yesMolecular & Cellular Oncology, 2019
Ataxia-telangiectasia-mutated (ATM) promotes homologous recombination (HR)-mediated DNA double-strand break repair. It was recently shown that the proteasomal shuttle factor UBQLN4 facilitates MRE11 degradation to repress HR.
Ron D. Jachimowicz   +1 more
doaj   +1 more source

Restricting the ligation step of non-homologous end-joining [PDF]

open access: yesDNA Repair, 2007
Non-homologous end-joining is an important pathway for repairing DNA double-strand breaks. The budding yeast Saccharomyces cerevisiae possesses two proteins, Nej1/Lif2 and Ntr1/Spp382, which play a role in restricting the activity of Dnl4-Lif1, the complex that executes the final ligation step of this process.
Miroslav, Chovanec, Thomas E, Wilson
openaire   +2 more sources

Dual roles for DNA polymerase theta in alternative end-joining repair of double-strand breaks in Drosophila.

open access: yesPLoS Genetics, 2010
DNA double-strand breaks are repaired by multiple mechanisms that are roughly grouped into the categories of homology-directed repair and non-homologous end joining.
Sze Ham Chan, Amy Marie Yu, Mitch McVey
doaj   +1 more source

Molecular Process Producing Oncogene Fusion in Lung Cancer Cells by Illegitimate Repair of DNA Double-Strand Breaks

open access: yesBiomolecules, 2015
Constitutive activation of oncogenes by fusion to partner genes, caused by chromosome translocation and inversion, is a critical genetic event driving lung carcinogenesis. Fusions of the tyrosine kinase genes ALK (anaplastic lymphoma kinase), ROS1 (c-ros
Yoshitaka Seki   +2 more
doaj   +1 more source

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