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Non-homologous end joining as a mechanism of DNA repair [PDF]

Current Biology, 2001
In a field where we are still identifying the key players, it is clear that there is much left to learn about non-homologous end joining as a mechanism of DNA repair. And any process acting on DNA must be considered in the broader context of chromatin conformation and sub-nuclear structure: there is clear evidence, largely from yeast, of interactions ...
openaire   +2 more sources

Repair Mechanisms of Non-Homologous End Joining.

, 2013
(A) The primary repair pathway of DSB repair by NHEJ is mediated by a hetrodimer DNA-PK which is made up of Ku70, Ku 80 and DNA-PKcs and is commonly named DNA-PK Dependant Non-Homologous End Joining (D-NHEJ). Once the DNA-PK has formed a complex with the
Graham Smith (279803), David Dolan (107443), Anze Zupanic (279802), Daryl Shanley (183695), Glyn Nelson (73268)   +4 more
core   +1 more source

Genome instability and pressure on non-homologous end joining drives chemotherapy resistance via a DNA repair crisis switch in triple negative breast cancer. [PDF]

, 2021
Chemotherapy is used as a standard-of-care against cancers that display high levels of inherent genome instability. Chemotherapy induces DNA damage and intensifies pressure on the DNA repair pathways that can lead to deregulation.
Adams, M.N., Wiegmans, A.P., Ward, Ambber, Kelly, Greg, Van Oosterhout, Romy, Ivanova, E., Lee, J.S., Van Oosterhout, R., Najib, I.M., Lee, Jason S, O'Byrne, Ken, Najib, Idris Mohd, O'Byrne, K., Duijf, Pascal H G, Sadowski, Martin C, Morrical, S.W., Morrical, Scott W, Richard, D.J., Duijf, P.H.G., Ivanova, Ekaterina, Adams, Mark N, Sadowski, M.C., Kelly, G., Wiegmans, Adrian P, Richard, Derek J, Ward, A.   +25 more
core   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

ATM limits incorrect end utilization during non-homologous end joining of multiple chromosome breaks.

PLoS Genetics, 2010
Chromosome rearrangements can form when incorrect ends are matched during end joining (EJ) repair of multiple chromosomal double-strand breaks (DSBs).
Nicole Bennardo, Jeremy M Stark
doaj   +1 more source

Human RAP1 inhibits non‐homologous end joining at telomeres [PDF]

The EMBO Journal, 2009
Telomeres, the nucleoprotein structures at the ends of linear chromosomes, promote genome stability by distinguishing chromosome termini from DNA double-strand breaks (DSBs). Cells possess two principal pathways for DSB repair: homologous recombination and non-homologous end joining (NHEJ).
Jay, Sarthy, Nancy S, Bae, Jonathan, Scrafford, Peter, Baumann   +3 more
openaire   +2 more sources

Alternative splicing in multiple myeloma is associated with the non-homologous end joining pathway

, 2023
Alternative splicing plays a pivotal role in tumorigenesis and proliferation. However, its pattern and pathogenic role has not been systematically analyzed in multiple myeloma or its subtypes. Alternative splicing profiles for 598 newly diagnosed myeloma
Enze Liu, Nathan Becker, Sudha, Parvathi, Dong, Chuanpeng, Morgan, Gareth, Keats, Jonathan, Chuanpeng Dong, Gareth Morgan, Liu, Yunlong, Jonathan Keats, Parvathi Sudha, Yunlong Liu, Brian A. Walker, Liu, Enze, Becker, Nathan, Walker, Brian A.   +15 more
core   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Structure of the Helicase Domain of DNA Polymerase Theta Reveals a Possible Role in the Microhomology-Mediated End-Joining Pathway

, 2015
DNA polymerase theta (Polθ) has been identified as a crucial alternative non-homologous end-joining factor in mammalian cells. Polθ is upregulated in a range of cancer cell types defective in homologous recombination, and knockdown has been shown to ...
Aitkenhead, H, Gileadi, Opher, Cooper, Christopher D O, Newman, JA, Cooper, CD, Gileadi, O, Cooper, Christopher D.O., Newman, Joseph A., Aitkenhead, Hazel   +8 more
core   +1 more source

DNA break site at fragile subtelomeres determines probability and mechanism of antigenic variation in African trypanosomes. [PDF]

, 2013
Antigenic variation in African trypanosomes requires monoallelic transcription and switching of variant surface glycoprotein (VSG) genes. The transcribed VSG, always flanked by '70 bp'-repeats and telomeric-repeats, is either replaced through DNA double ...
Glover, Lucy, Horn, David, Horn, David; id_orcid, Lucy Glover (24966), Sam Alsford, David Horn (24969), Alsford, Sam, Lucy Glover, Sam Alsford (24967), David Horn   +9 more
core   +1 more source