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15
BRIEF COMMUNICATION Cisplatin Resistance Conferred by the RAD51D (E233G) Genetic Variant Is Dependent Upon p53
, 2016
"... All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately. ..."
Abstract
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All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately.
C-terminal domain with
, 2006
"... RAD51AP2, a novel vertebrate- and meiotic-specific protein, shares a conserved RAD51-interacting ..."
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RAD51AP2, a novel vertebrate- and meiotic-specific protein, shares a conserved RAD51-interacting
unknown title
, 2006
"... RAD51AP2, a novel vertebrate- and meiotic-specific protein, shares a conserved RAD51-interacting C-terminal domain with RAD51AP1/PIR51 ..."
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RAD51AP2, a novel vertebrate- and meiotic-specific protein, shares a conserved RAD51-interacting C-terminal domain with RAD51AP1/PIR51
unknown title
, 2007
"... BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage ..."
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BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage
Use of the HPRT gene to study nuclease-induced DNA double-strand break repair
"... Abstract Understanding the mechanisms of chromosomal double-strand break repair (DSBR) provides insight into genome instability, oncogenesis and genome engineering, including disease gene correction. Research into DSBR exploits rare-cutting endonucleases to cleave exogenous reporter constructs inte ..."
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Abstract Understanding the mechanisms of chromosomal double-strand break repair (DSBR) provides insight into genome instability, oncogenesis and genome engineering, including disease gene correction. Research into DSBR exploits rare-cutting endonucleases to cleave exogenous reporter constructs integrated into the genome. Multiple reporter constructs have been developed to detect various DSBR pathways. Here, using a single endogenous reporter gene, the X-chromosomal disease gene encoding hypoxanthine phosphoribosyltransferase (HPRT), we monitor the relative utilization of three DSBR pathways following cleavage by I-SceI or CRISPR/Cas9 nucleases. For I-SceI, our estimated frequencies of accurate or mutagenic nonhomologous end-joining and gene correction by homologous recombination are 4.1, 1.5 and 0.16%, respectively. Unexpectedly, I-SceI and Cas9 induced markedly different DSBR profiles. Also, using an I-SceI-sensitive HPRT minigene, we show that gene correction is more efficient when using long double-stranded DNA than single-or double-stranded oligonucleotides. Finally, using both endogenous HPRT and exogenous reporters, we validate novel cell cycle phase-specific I-SceI derivatives for investigating cell cycle variations in DSBR. The results obtained using these novel approaches provide new insights into template design for gene correction and the relationships between multiple DSBR pathways at a single endogenous disease gene.
unknown title
, 2007
"... BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage ..."
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BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage
unknown title
, 2007
"... BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage ..."
Abstract
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BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage
