scholarly journals Triphlorethol-A Improves the Non-Homologous End Joining and Base-Excision Repair Capacity Impaired by Formaldehyde

2011 ◽  
Vol 74 (12) ◽  
pp. 811-821 ◽  
Author(s):  
Rui Zhang ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Ki Cheon Kim ◽  
Nam Ho Lee ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
End Joining ◽  
Repair Capacity ◽  
Base Excision ◽  
Non Homologous End Joining

scholarly journals Investigations on the role of base excision repair and non-homologous end-joining pathways in sodium selenite-induced toxicity and mutagenicity in Saccharomyces cerevisiae

Mutagenesis ◽  
2009 ◽  
Vol 25 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Dominika Mániková ◽  
Danuša Vlasáková ◽  
Jana Loduhová ◽  
Lucia Letavayová ◽  
Dana Vigašová ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Base Excision Repair ◽  
Sodium Selenite ◽  
Excision Repair ◽  
End Joining ◽  
Base Excision ◽  
Non Homologous End Joining

scholarly journals Variation in base excision repair capacity

2011 ◽  
Vol 711 (1-2) ◽  
pp. 100-112 ◽  
Author(s):  
David M. Wilson ◽  
Daemyung Kim ◽  
Brian R. Berquist ◽  
Alice J. Sigurdson
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Repair Capacity ◽  
Base Excision

scholarly journals Base excision repair capacity in informing healthspan

2014 ◽  
Vol 35 (12) ◽  
pp. 2643-2652 ◽  
Author(s):  
B. M. Brenerman ◽  
J. L. Illuzzi ◽  
D. M. Wilson
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Repair Capacity ◽  
Base Excision

scholarly journals Somatic Mutations in Oncogenes Are in Chronic Myeloid Leukemia Acquired De Novo via Deregulated Base-Excision Repair and Alternative Non-Homologous End Joining

2021 ◽  
Vol 11 ◽  
Author(s):  
Nikola Curik ◽  
Vaclava Polivkova ◽  
Pavel Burda ◽  
Jitka Koblihova ◽  
Adam Laznicka ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Base Excision Repair ◽  
Myeloid Leukemia ◽  
Somatic Mutations ◽  
De Novo ◽  
Excision Repair ◽  
Leukemic Cells ◽  
End Joining ◽  
Base Excision

Somatic mutations are a common molecular mechanism through which chronic myeloid leukemia (CML) cells acquire resistance to tyrosine kinase inhibitors (TKIs) therapy. While most of the mutations in the kinase domain of BCR-ABL1 can be successfully managed, the recurrent somatic mutations in other genes may be therapeutically challenging. Despite the major clinical relevance of mutation-associated resistance in CML, the mechanisms underlying mutation acquisition in TKI-treated leukemic cells are not well understood. This work demonstrated de novo acquisition of mutations on isolated single-cell sorted CML clones growing in the presence of imatinib. The acquisition of mutations was associated with the significantly increased expression of the LIG1 and PARP1 genes involved in the error-prone alternative nonhomologous end-joining pathway, leading to genomic instability, and increased expression of the UNG, FEN and POLD3 genes involved in the base-excision repair (long patch) pathway, allowing point mutagenesis. This work showed in vitro and in vivo that de novo acquisition of resistance-associated mutations in oncogenes is the prevalent method of somatic mutation development in CML under TKIs treatment.

DNA repair and genomic stability

2019 ◽  
pp. 173-183
Author(s):  
John C. Lucchesi
Keyword(s):  
Excision Repair ◽  
Strand Break ◽  
End Joining ◽  
Single Strand Break ◽  
Dna Mismatch ◽  
Single Strand Break Repair ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Base Excision ◽  
Non Homologous End Joining

A number of pathways have evolved in order to repair DNA. Mismatch repair (MMR) operates when an improper nucleotide is used or when an insertion or deletion occurs during replication. Nucleotide excision repair (NER) repairs damage that distorts the DNA helix such as the presence of pyrimidine dimers induced by ultraviolet light. Base excision repair (BER) removes damaged or altered DNA bases that do not result in a conformational change in the chromatin. Single-strand break repair (SSBR) uses the same enzymatic steps as BER. Double-strand break (DSB) repair can involve either non-homologous end-joining (NHEJ) or homologous recombination (HR). In NHEJ, the broken DNA ends are joined directly. HR requires that one of the strands of the broken DNA molecule participates in the strand invasion of the sister chromatid. The site of the DSB must be modified to allow access to the repair machinery. This modification involves remodeling complexes, as well as histone-modifying enzymes.

scholarly journals Nonhomologous end joining of complex DNA double-strand breaks with proximal thymine glycol and interplay with base excision repair

DNA Repair ◽  
2016 ◽  
Vol 41 ◽  
pp. 16-26 ◽  
Author(s):  
Mohammed Almohaini ◽  
Sri Lakshmi Chalasani ◽  
Duaa Bafail ◽  
Konstantin Akopiants ◽  
Tong Zhou ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Double Strand Breaks ◽  
Nonhomologous End Joining ◽  
Dna Double Strand Breaks ◽  
End Joining ◽  
Strand Breaks ◽  
Thymine Glycol ◽  
Base Excision

Base excision repair capacity in chronic renal failure patients undergoing hemodialysis treatment

2013 ◽  
Vol 32 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Elitsa Stoyanova ◽  
Susana Pastor ◽  
Elisabet Coll ◽  
Amaya Azqueta ◽  
Andrew R. Collins ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Repair Capacity ◽  
Hemodialysis Treatment ◽  
Base Excision

Base excision repair capacity as a determinant of prognosis and therapy response in colon cancer patients

DNA Repair ◽  
2018 ◽  
Vol 72 ◽  
pp. 77-85 ◽  
Author(s):  
Sona Vodenkova ◽  
Katerina Jiraskova ◽  
Marketa Urbanova ◽  
Michal Kroupa ◽  
Jana Slyskova ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Patients ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Therapy Response ◽  
Repair Capacity ◽  
Base Excision
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