Triplex technology in studies of DNA damage, DNA repair, and mutagenesis

Mukherjee, Anirban; Vásquez, Karen M.

doi:10.1016/j.biochi.2011.04.001

Cited by 77 publications

(66 citation statements)

References 159 publications

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“…Specificity can be determined either by Watson-Crick base pairing or, in the case of triplex forming oligonucleotides (TFOs), by formation of a non-canonical triple helical structure (Mukherjee and Vasquez, 2011). Additionally, the targeting oligonucleotide can itself be used as the donor molecule for gene correction or two oligonucleotides can be used, one to target the lesion and one as donor.…”

Section: Rare-cutting Endonucleases Natural and Engineeredmentioning

confidence: 99%

Targeted gene therapies: tools, applications, optimization

Humbert

Davis

Maizels

2012

Critical Reviews in Biochemistry and Molecular Biology

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Many devastating human diseases are caused by mutations in a single gene that prevent a somatic cell from carrying out its essential functions, or by genetic changes acquired as a result of infectious disease or in the course of cell transformation. Targeted gene therapies have emerged as potential strategies for treatment of such diseases. These therapies depend upon rare-cutting endonucleases to cleave at specific sites in or near disease genes. Targeted gene correction provides a template for homology-directed repair, enabling the cell's own repair pathways to erase the mutation and replace it with the correct sequence. Targeted gene disruption ablates the disease gene, disabling its function. Gene targeting can also promote other kinds of genome engineering, including mutation, insertion, or gene deletion. Targeted gene therapies present significant advantages compared to approaches to gene therapy that depend upon delivery of stably expressing transgenes. Recent progress has been fueled by advances in nuclease discovery and design, and by new strategies that maximize efficiency of targeting and minimize off-target damage. Future progress will build on deeper mechanistic understanding of critical factors and pathways.

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Section: Rare-cutting Endonucleases Natural and Engineeredmentioning

confidence: 99%

Targeted gene therapies: tools, applications, optimization

Humbert

Davis

Maizels

2012

Critical Reviews in Biochemistry and Molecular Biology

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“…Besides, the single-stranded area, or the triplex region is also a target of various nucleases, resulting in single or DSBs formation, and the increased mutagenesis or recombination (Wang & Vasquez, 2006). Although triplex (H-DNA) DNA occurs mainly at poly (purine·pyrimidine) ((R·Y) n ) tracts, it can also be induced to form with the sequence specific DNA recognition and binding of some synthetic triplex-forming oligonucleotides (TFOs) (Casey & Glazer, 2001;Mukherjee & Vasquez, 2011). TFOs bind to the major groove of homopurine-homopyrimidine stretches of double-stranded DNA to induce forming the triplex (Casey & Glazer, 2001;Mukherjee & Vasquez, 2011).…”

Section: H-dna and H-dna Induced Dsbs And Genetic Instabilitymentioning

confidence: 99%

“…Although triplex (H-DNA) DNA occurs mainly at poly (purine·pyrimidine) ((R·Y) n ) tracts, it can also be induced to form with the sequence specific DNA recognition and binding of some synthetic triplex-forming oligonucleotides (TFOs) (Casey & Glazer, 2001;Mukherjee & Vasquez, 2011). TFOs bind to the major groove of homopurine-homopyrimidine stretches of double-stranded DNA to induce forming the triplex (Casey & Glazer, 2001;Mukherjee & Vasquez, 2011). During which the duplex DNA may have to undergo helical distortions on TFO binding and the distortions trigger endogenous recombination and repair mechanisms in the cell (Raghavan et al, 2004(Raghavan et al, , 2005.…”

Section: H-dna and H-dna Induced Dsbs And Genetic Instabilitymentioning

confidence: 99%

The Gratuitous Repair on Undamaged DNA Misfold

Pan¹,

Xiao²,

Hong-qun³

et al. 2011

DNA Repair

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“…Therefore, the site specific and stable triplex DNA formation for the target duplex DNA is anticipated to become an important method for the gene targeting technologies and therapies as an antigene method. [1][2][3][4][5] The triplex DNA is formed by the interaction between the triplex forming oligonucleotides (TFOs) and the homopurine region within the duplex DNA. 6) Triplex DNAs are classified into two types according to the orientation of the phosphate backbone of the TFOs.…”

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Stable and Selective Antiparallel Type Triplex DNA Formation by Targeting a GC Base Pair with the TFO Containing One <i>N</i><sup>2</sup>-Phenyl-2′-deoxyguanosine

Taniguchi

Miyazaki

Matsueda

et al. 2018

CHEMICAL & PHARMACEUTICAL BULLETIN

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The antiparallel triplex DNA is formed by the interaction between purine-rich triplex forming oligonucleotides (TFOs) and the homo-purine region within a duplex DNA. The formation of such a structure with the genome DNA promises to control the gene expression in a living cell. In this study, in an attempt to enhance the stability of the triplex DNAs, we have designed the N 2 -arylated deoxyguanosine derivatives. Among these analogues, we found that the TFOs containing N 2 -phenyl-2′-deoxyguanosine (PhdG) showed a stable and selective triplex DNA formation with the GC base pair as compared to the natural dG/GC triplet. However, the multiple incorporation of PhdG into the TFOs hampered the stable triplex DNA, instead, showed a tendency to form a higher order structure. Therefore, we concluded that the stable and selective triplex DNA formation is expected by the replacement of dG by PhdG in the purine-rich TFO sequence. Key words N2 -arylated deoxyguanosine; triplex forming oligonucleotide; triplex DNA By forming the triplex DNA versus the duplex DNA, it is possible to control the gene expression, gene recombination, gene repair, etc. Therefore, the site specific and stable triplex DNA formation for the target duplex DNA is anticipated to become an important method for the gene targeting technologies and therapies as an antigene method.1-5) The triplex DNA is formed by the interaction between the triplex forming oligonucleotides (TFOs) and the homopurine region within the duplex DNA.6) Triplex DNAs are classified into two types according to the orientation of the phosphate backbone of the TFOs. The antiparallel type triplex DNA is formed under neutral conditions, in which the TFOs composed of deoxyguanosine (dG) and deoxyadenosine (dA) form two hydrogen bonds in the guanine base of the GC base pair and the adenine base of the AT base pair of the duplex DNA, respectively, in an antiparallel orientation regarding the homopurine strand of the duplex DNA (Fig. 1A). On the other hand, the TFOs composed of deoxycytosine (dC) and thymidine (T) forms two hydrogen bond in the guanine base and adenine base of the homopurine strand in a parallel orientation, respectively. As the protonated cytidine is included in the parallel type triplex, its formation requires acidic conditions (Fig. 1B). To date, we have developed the artificial nucleoside analogues to form the nonnatural and antiparallel type triplex DNA for the duplex DNA containing the CG and TA base pair to expand the triplex recognition code.7-12) However, improvement of the stability of the antiparallel type triplex DNA by an artificial nucleic acid is a still challenging issue.The stacking interaction has been shown to be more effective with the triplex DNA than with the duplex DNA. For example, adriamycin and actinomycin, having a high aromaticity, are known to interact with the duplex DNA, but have a rather high binding ability to the triplex DNA.13) Moreover, the duplex DNA containing N 2 -phenyldeoxyguanosine (PhdG) showed a slightly higher thermal melting temp...

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Triplex technology in studies of DNA damage, DNA repair, and mutagenesis

Cited by 77 publications

References 159 publications

Targeted gene therapies: tools, applications, optimization

Targeted gene therapies: tools, applications, optimization

The Gratuitous Repair on Undamaged DNA Misfold

Stable and Selective Antiparallel Type Triplex DNA Formation by Targeting a GC Base Pair with the TFO Containing One <i>N</i><sup>2</sup>-Phenyl-2′-deoxyguanosine

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