Research output: Contribution to journal › Review article › peer-review
Base Excision DNA Repair Deficient Cells : From Disease Models to Genotoxicity Sensors. / Kim, Daria V.; Makarova, Alena V.; Miftakhova, Regina R. et al.
In: Current Pharmaceutical Design, Vol. 25, No. 3, 01.01.2019, p. 298-312.Research output: Contribution to journal › Review article › peer-review
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TY - JOUR
T1 - Base Excision DNA Repair Deficient Cells
T2 - From Disease Models to Genotoxicity Sensors
AU - Kim, Daria V.
AU - Makarova, Alena V.
AU - Miftakhova, Regina R.
AU - Zharkov, Dmitry O.
N1 - Publisher Copyright: © 2019 Bentham Science Publishers.
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Base excision DNA repair (BER) is a vitally important pathway that protects the cell genome from many kinds of DNA damage, including oxidation, deamination, and hydrolysis. It involves several tightly coordinated steps, starting from damaged base excision and followed by nicking one DNA strand, incorporating an undamaged nucleotide, and DNA ligation. Deficiencies in BER are often embryonic lethal or cause morbid diseases such as cancer, neurodegeneration, or severe immune pathologies. Starting from the early 1980s, when the first mammalian cell lines lacking BER were produced by spontaneous mutagenesis, such lines have become a treasure trove of valuable information about the mechanisms of BER, often revealing unexpected connections with other cellular processes, such as antibody maturation or epigenetic demethylation. In addition, these cell lines have found an increasing use in genotoxicity testing, where they provide increased sensitivity and representativity to cell-based assay panels. In this review, we outline current knowledge about BER-deficient cell lines and their use.
AB - Base excision DNA repair (BER) is a vitally important pathway that protects the cell genome from many kinds of DNA damage, including oxidation, deamination, and hydrolysis. It involves several tightly coordinated steps, starting from damaged base excision and followed by nicking one DNA strand, incorporating an undamaged nucleotide, and DNA ligation. Deficiencies in BER are often embryonic lethal or cause morbid diseases such as cancer, neurodegeneration, or severe immune pathologies. Starting from the early 1980s, when the first mammalian cell lines lacking BER were produced by spontaneous mutagenesis, such lines have become a treasure trove of valuable information about the mechanisms of BER, often revealing unexpected connections with other cellular processes, such as antibody maturation or epigenetic demethylation. In addition, these cell lines have found an increasing use in genotoxicity testing, where they provide increased sensitivity and representativity to cell-based assay panels. In this review, we outline current knowledge about BER-deficient cell lines and their use.
KW - base excision repair
KW - DNA repair
KW - epigenetic demethylation
KW - genotoxicity assays
KW - knockout cell lines
KW - mutagenesis.
KW - SOMATIC HYPERMUTATION
KW - STRAND-BREAK REPAIR
KW - POLYMERASE THETA POLQ
KW - mutagenesis
KW - MICE LACKING
KW - LIGASE I DEFICIENCY
KW - LYASE ACTIVITY
KW - OXIDATIVELY MODIFIED BASE
KW - CATALYTIC-ACTIVITY
KW - LONG-PATCH REPAIR
KW - ADENOMATOUS POLYPOSIS
KW - Humans
KW - DNA Glycosylases
KW - DNA-Directed DNA Polymerase
KW - Cell Line
KW - DNA Ligases
KW - Animals
KW - DNA
KW - DNA Repair
KW - Endonucleases
KW - DNA Damage
KW - Knockout cell lines
KW - Base excision repair
KW - Epigenetic demethylation
KW - Dna repair
KW - Genotoxicity assays
KW - Mutagenesis
UR - http://www.scopus.com/inward/record.url?scp=85068188849&partnerID=8YFLogxK
U2 - 10.2174/1381612825666190319112930
DO - 10.2174/1381612825666190319112930
M3 - Review article
C2 - 31198112
AN - SCOPUS:85068188849
VL - 25
SP - 298
EP - 312
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
SN - 1381-6128
IS - 3
ER -
ID: 20710364