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Journal articles on the topic 'Nickase'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 April 2022

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1

He, Yan, and Tao Jiang. "Nickase-dependent isothermal DNA amplification." Advances in Bioscience and Biotechnology 04, no. 04 (2013): 539–42. http://dx.doi.org/10.4236/abb.2013.44070.

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2

Wu, Haibo, Yongsheng Wang, Yan Zhang, Mingqi Yang, Jiaxing Lv, Jun Liu, and Yong Zhang. "TALE nickase-mediatedSP110knockin endows cattle with increased resistance to tuberculosis." Proceedings of the National Academy of Sciences 112, no. 13 (March 2, 2015): E1530—E1539. http://dx.doi.org/10.1073/pnas.1421587112.

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Transcription activator-like effector nuclease (TALEN)-mediated genome modification has been applied successfully to create transgenic animals in various species, such as mouse, pig, and even monkey. However, transgenic cattle with gene knockin have yet to be created using TALENs. Here, we report site-specific knockin of the transcription activator-like effector (TALE) nickase-mediated SP110 nuclear body protein gene (SP110) via homologous recombination to produce tuberculosis-resistant cattle. In vitro and in vivo challenge and transmission experiments proved that the transgenic cattle are able to control the growth and multiplication ofMycobacterium bovis, turn on the apoptotic pathway of cell death instead of necrosis after infection, and efficiently resist the low dose ofM.bovistransmitted from tuberculous cattle in nature. In this study, we developed TALE nickases to modify the genome of Holstein–Friesian cattle, thereby engineering a heritable genome modification that facilitates resistance to tuberculosis.
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3

Kim, Do Yon, Su Bin Moon, Jeong-Heon Ko, Yong-Sam Kim, and Daesik Kim. "Unbiased investigation of specificities of prime editing systems in human cells." Nucleic Acids Research 48, no. 18 (September 17, 2020): 10576–89. http://dx.doi.org/10.1093/nar/gkaa764.

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Abstract Prime editors (PEs) enable targeted precise editing, including the generation of substitutions, insertions and deletions, in eukaryotic genomes. However, their genome-wide specificity has not been explored. Here, we developed Nickase-based Digenome-seq (nDigenome-seq), an in vitro assay that uses whole-genome sequencing to identify single-strand breaks induced by CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 (CRISPR-associated protein 9) nickase. We used nDigenome-seq to screen for potential genome-wide off-target sites of Cas9 H840A nickase, a PE component, targeted to nine human genomic sites. Then, using targeted amplicon sequencing of off-target candidates identified by nDigenome-seq, we showed that only five off-target sites showed detectable PE-induced modifications in cells, at frequencies ranging from 0.1 to 1.9%, suggesting that PEs provide a highly specific method of precise genome editing. We also found that PE specificity in human cells could be further improved by incorporating mutations from engineered Cas9 variants, particularly eSpCas9 and Sniper Cas9, into PE.
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4

Jansson, Vuokko, and Kristian Jansson. "A bioluminescent DNA nickase assay of deoxyribonuclease I." Analytical Biochemistry 333, no. 2 (October 2004): 402–4. http://dx.doi.org/10.1016/j.ab.2004.05.060.

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5

Yunusova, A. K., E. A. Rogulin, R. I. Artyukh, L. A. Zheleznaya, and N. I. Matvienko. "Nickase and a protein encoded by an open reading frame downstream from the nickase BspD6I gene form a restriction endonuclease complex." Biochemistry (Moscow) 71, no. 7 (July 2006): 815–20. http://dx.doi.org/10.1134/s0006297906070157.

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6

Davis, Luther, and Nancy Maizels. "Homology-directed repair of DNA nicks via pathways distinct from canonical double-strand break repair." Proceedings of the National Academy of Sciences 111, no. 10 (February 20, 2014): E924—E932. http://dx.doi.org/10.1073/pnas.1400236111.

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DNA nicks are the most common form of DNA damage, and if unrepaired can give rise to genomic instability. In human cells, nicks are efficiently repaired via the single-strand break repair pathway, but relatively little is known about the fate of nicks not processed by that pathway. Here we show that homology-directed repair (HDR) at nicks occurs via a mechanism distinct from HDR at double-strand breaks (DSBs). HDR at nicks, but not DSBs, is associated with transcription and is eightfold more efficient at a nick on the transcribed strand than at a nick on the nontranscribed strand. HDR at nicks can proceed by a pathway dependent upon canonical HDR factors RAD51 and BRCA2; or by an efficient alternative pathway that uses either ssDNA or nicked dsDNA donors and that is strongly inhibited by RAD51 and BRCA2. Nicks generated by either I-AniI or the CRISPR/Cas9D10A nickase are repaired by the alternative HDR pathway with little accompanying mutagenic end-joining, so this pathway may be usefully applied to genome engineering. These results suggest that alternative HDR at nicks may be stimulated in physiological contexts in which canonical RAD51/BRCA2-dependent HDR is compromised or down-regulated, which occurs frequently in tumors.
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7

Ren, Xingjie, Zhihao Yang, Decai Mao, Zai Chang, Huan-Huan Qiao, Xia Wang, Jin Sun, et al. "Performance of the Cas9 Nickase System in Drosophila melanogaster." G3: Genes|Genomes|Genetics 4, no. 10 (August 15, 2014): 1955–62. http://dx.doi.org/10.1534/g3.114.013821.

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8

Christensen, Jesper, Susan F. Cotmore, and Peter Tattersall. "Minute Virus of Mice Initiator Protein NS1 and a Host KDWK Family Transcription Factor Must Form a Precise Ternary Complex with Origin DNA for Nicking To Occur." Journal of Virology 75, no. 15 (August 1, 2001): 7009–17. http://dx.doi.org/10.1128/jvi.75.15.7009-7017.2001.

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ABSTRACT Parvoviral rolling hairpin replication generates palindromic genomic concatemers whose junctions are resolved to give unit-length genomes by a process involving DNA replication initiated at origins derived from each viral telomere. The left-end origin of minute virus of mice (MVM), oriL, contains binding sites for the viral initiator nickase, NS1, and parvovirus initiation factor (PIF), a member of the emerging KDWK family of transcription factors. oriL is generated as an active form, oriLTC, and as an inactive form, oriLGAA, which contains a single additional nucleotide inserted between the NS1 and PIF sites. Here we examined the interactions on oriLTC which lead to activation of NS1 by PIF. The two subunits of PIF, p79 and p96, cooperatively bind two ACGT half-sites, which can be flexibly spaced. When coexpressed from recombinant baculoviruses, the PIF subunits preferentially form heterodimers which, in the presence of ATP, show cooperative binding with NS1 on oriL, but this interaction is preferentially enhanced on oriLTC compared to oriLGAA. Without ATP, NS1 is unable to bind stably to its cognate site, but PIF facilitates this interaction, rendering the NS1 binding site, but not the nick site, resistant to DNase I. Varying the spacing of the PIF half-sites shows that the distance between the NS1 binding site and the NS1-proximal half-site is critical for nickase activation, whereas the position of the distal half-site is unimportant. When expressed separately, both PIF subunits form homodimers that bind site specifically to oriL, but only complexes containing p79 activate the NS1 nickase function.
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9

Nüesch, Jürg P. F., Jesper Christensen, and Jean Rommelaere. "Initiation of Minute Virus of Mice DNA Replication Is Regulated at the Level of Origin Unwinding by Atypical Protein Kinase C Phosphorylation of NS1." Journal of Virology 75, no. 13 (July 1, 2001): 5730–39. http://dx.doi.org/10.1128/jvi.75.13.5730-5739.2001.

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ABSTRACT Minute virus of mice nonstructural protein NS1 is a multifunctional protein that is involved in many processes necessary for virus propagation. To perform its distinct activities in timely coordinated manner, NS1 was suggested to be regulated by posttranslational modifications, in particular phosphorylation. In fact, NS1 replicative functions are dependent on protein kinase C (PKC) phosphorylation, most likely due to alteration of the biochemical profile of the viral product as determined by comparing native NS1 with its dephosphorylated counterpart. Through the characterization of NS1 mutants at individual PKC consensus phosphorylation sites for their biochemical activities and nickase function, we were able to identify two target atypical PKC phosphorylation sites, T435 and S473, serving as regulatory elements for the initiation of viral DNA replication. Furthermore, by dissociating the energy-dependent helicase activity from the ATPase-independent trans esterification reaction using partially single-stranded substrates, we could demonstrate that atypical PKC regulation of NS1 nickase activity occurs at the level of origin unwinding prior to trans esterification.
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10

Liebendorfer, Adam. "Novel Cas9-nickase technique repairs mutation without off-target modifications." Scilight 2018, no. 49 (December 3, 2018): 490001. http://dx.doi.org/10.1063/1.5082920.

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11

Xu, Tao, Yongchao Li, Zhou Shi, Christopher L. Hemme, Yuan Li, Yonghua Zhu, Joy D. Van Nostrand, Zhili He, and Jizhong Zhou. "Efficient Genome Editing in Clostridium cellulolyticum via CRISPR-Cas9 Nickase." Applied and Environmental Microbiology 81, no. 13 (April 24, 2015): 4423–31. http://dx.doi.org/10.1128/aem.00873-15.

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ABSTRACTThe CRISPR-Cas9 system is a powerful and revolutionary genome-editing tool for eukaryotic genomes, but its use in bacterial genomes is very limited. Here, we investigated the use of theStreptococcus pyogenesCRISPR-Cas9 system in editing the genome ofClostridium cellulolyticum, a model microorganism for bioenergy research. Wild-type Cas9-induced double-strand breaks were lethal toC. cellulolyticumdue to the minimal expression of nonhomologous end joining (NHEJ) components in this strain. To circumvent this lethality, Cas9 nickase was applied to develop a single-nick-triggered homologous recombination strategy, which allows precise one-step editing at intended genomic loci by transforming a single vector. This strategy has a high editing efficiency (>95%) even using short homologous arms (0.2 kb), is able to deliver foreign genes into the genome in a single step without a marker, enables precise editing even at two very similar target sites differing by two bases preceding the seed region, and has a very high target site density (median interval distance of 9 bp and 95.7% gene coverage inC. cellulolyticum). Together, these results establish a simple and robust methodology for genome editing in NHEJ-ineffective prokaryotes.
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12

Kim, Gap‐Don, Jeong Hyo Lee, Sumin Song, Seo Woo Kim, Ji Seon Han, Seung Pyo Shin, Byung‐Chul Park, and Tae Sub Park. "Generation of myostatin‐knockout chickens mediated by D10A‐Cas9 nickase." FASEB Journal 34, no. 4 (February 25, 2020): 5688–96. http://dx.doi.org/10.1096/fj.201903035r.

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13

Molina, Rafael, María José Marcaida, Pilar Redondo, Marco Marenchino, Phillippe Duchateau, Marco D'Abramo, Guillermo Montoya, and Jesús Prieto. "Engineering a Nickase on the Homing Endonuclease I-DmoI Scaffold." Journal of Biological Chemistry 290, no. 30 (June 4, 2015): 18534–44. http://dx.doi.org/10.1074/jbc.m115.658666.

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14

Shao, Yanjiao, Liren Wang, Nana Guo, Shengfei Wang, Lei Yang, Yajing Li, Mingsong Wang, et al. "Cas9-nickase–mediated genome editing corrects hereditary tyrosinemia in rats." Journal of Biological Chemistry 293, no. 18 (March 5, 2018): 6883–92. http://dx.doi.org/10.1074/jbc.ra117.000347.

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15

Tomita, Haruyoshi, and Yasuyoshi Ike. "Genetic Analysis of Transfer-Related Regions of the Vancomycin Resistance Enterococcus Conjugative Plasmid pHTβ: Identification of oriT and a Putative Relaxase Gene." Journal of Bacteriology 187, no. 22 (November 15, 2005): 7727–37. http://dx.doi.org/10.1128/jb.187.22.7727-7737.2005.

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ABSTRACT The pHT plasmids pHTα (65.9 kbp), pHTβ (63.7 kbp), and pHTγ (66.5 kbp) are highly conjugative pheromone-independent pMG1-like plasmids that carry Tn1546-like transposons encoding vancomycin resistance. pHTβ is the prototype plasmid, and the pHTα and pHTγ plasmids are derivatives of the insertion into pHTβ of an IS232-like (2.2 kbp) element and a group II intron (2.8 kbp), respectively. The complete nucleotide sequence of the pHTβ plasmid was determined and, with the exception of the Tn1546-like insertion (10,851 bp), was found to be 52,890 bp. Sixty-one open reading frames (ORFs) having the same transcript orientation were identified. A homology search revealed that 22 of the pHTβ (pHT) plasmid ORFs showed similarities to the ORFs identified on the pXO2 plasmid (96.2 kbp), which is the virulence plasmid essential for capsule formation by Bacillus anthracis; however, the functions of most of the ORFs remain unknown. Most other ORFs did not show any significant homology to reported genes for which functions have been analyzed. To investigate the highly efficient transfer mechanism of the pHT plasmid, mutations with 174 unique insertions of transposon Tn917-lac insertion mutants of pHTβ were obtained. Of the 174 derivatives, 92 showed decrease or loss in transfer frequency, and 74 showed normal transfer frequency and LacZ expression. Eight derivatives showed normal transfer and no LacZ expression. Inserts within the 174 derivatives were mapped to 124 different sites on pHTβ. The Tn917-lac insertions which resulted in altered transfer frequency mapped to three separate regions designated I, II, and III, which were separated by segments in which insertions of Tn917-lac did not affect transfer. There was no region homologous to the previously reported oriT sequences in the pHT plasmid. The oriT was cloned by selection for the ability to mobilize the vector plasmid pAM401. The oriT region resided in a noncoding region (192 bp) between ORF31 and ORF32 and contained three direct repeat sequences and two inverted repeat sequences. ORF34, encoding a 506-amino-acid protein which was located downstream of the oriT region, contains the three conserved motifs (I to III) of the DNA relaxase/nickase of mobile plasmids. The transfer abilities of the Tn917-lac-insertion mutants of ORF34 or a mutant of ORF34 with an in-frame motif III deletion were completely abolished. The sequence of the oriT region and the deduced relaxase/nickase protein of ORF34 showed no significant similarity to the oriT and relaxase/nickase of other conjugative plasmids, respectively. The putative relaxase/nickase protein of ORF34 could be classified as a new member of the MOBMG family.
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16

Henderson, Dorian, and Richard Meyer. "The MobA-Linked Primase Is the Only Replication Protein of R1162 Required for Conjugal Mobilization." Journal of Bacteriology 181, no. 9 (May 1, 1999): 2973–78. http://dx.doi.org/10.1128/jb.181.9.2973-2978.1999.

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ABSTRACT Cells newly transformed with plasmid R1162 DNA were used as donors in conjugal matings to determine if the plasmid replication genes are necessary for transfer. An intact system for vegetative replication is not required for transfer at normal frequency, but the plasmid primase, in the form linked to the nickase, must be present in donor cells.
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17

Zargar, Mahsa, Abbas Jamshidizad, Aidin Rahim-Tayefeh, Ehsan Hashemi, Ali Najafi, Mehdi Shamsara, and Mohammad Hossein Modarressi. "Generation of global Spata19 knockout mouse using CRISPR/Cas9 nickase technology." Koomesh journal 22, no. 3 (May 1, 2020): 380–88. http://dx.doi.org/10.29252/koomesh.22.3.380.

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18

Shao, Yanjiao, Liren Wang, Nana Guo, Shengfei Wang, Lei Yang, Yajing Li, Mingsong Wang, et al. "Correction: Cas9-nickase–mediated genome editing corrects hereditary tyrosinemia in rats." Journal of Biological Chemistry 294, no. 21 (May 24, 2019): 8348. http://dx.doi.org/10.1074/jbc.aac119.009120.

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19

Pemberton, I. K., and J. S. Oxford. "4-Quinolones do not inhibit the nickase activity of HIV integrase." Antiviral Research 15 (April 1991): 72. http://dx.doi.org/10.1016/0166-3542(91)90139-i.

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20

Kachalova, Galina S., Eugeny A. Rogulin, Rimma I. Artyukh, Tatyana A. Perevyazova, Ludmila A. Zheleznaya, Nickolay I. Matvienko, and Hans D. Bartunik. "Crystallization and preliminary crystallographic analysis of the site-specific DNA nickase Nb.BspD6I." Acta Crystallographica Section F Structural Biology and Crystallization Communications 61, no. 3 (March 1, 2005): 332–34. http://dx.doi.org/10.1107/s174430910500309x.

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21

Fu, Becky Xu Hua, Justin D. Smith, Ryan T. Fuchs, Megumu Mabuchi, Jennifer Curcuru, G. Brett Robb, and Andrew Z. Fire. "Target-dependent nickase activities of the CRISPR–Cas nucleases Cpf1 and Cas9." Nature Microbiology 4, no. 5 (March 4, 2019): 888–97. http://dx.doi.org/10.1038/s41564-019-0382-0.

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22

Satomura, Atsushi, Kouichi Kuroda, and Mitsuyoshi Ueda. "Precise genome editing at single-base resolution by novel CRISPR-nickase system." New Biotechnology 33 (July 2016): S64—S65. http://dx.doi.org/10.1016/j.nbt.2016.06.947.

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23

Fujii, T., D. Naka, N. Toyoda, and H. Seto. "LiCl treatment releases a nickase implicated in genetic transformation of Streptococcus pneumoniae." Journal of Bacteriology 169, no. 11 (1987): 4901–6. http://dx.doi.org/10.1128/jb.169.11.4901-4906.1987.

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24

Wang, Ting, Yong Liu, Huan‐Huan Sun, Bin‐Cheng Yin, and Bang‐Ce Ye. "An RNA‐Guided Cas9 Nickase‐Based Method for Universal Isothermal DNA Amplification." Angewandte Chemie International Edition 58, no. 16 (April 8, 2019): 5382–86. http://dx.doi.org/10.1002/anie.201901292.

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25

Wang, Ting, Yong Liu, Huan‐Huan Sun, Bin‐Cheng Yin, and Bang‐Ce Ye. "An RNA‐Guided Cas9 Nickase‐Based Method for Universal Isothermal DNA Amplification." Angewandte Chemie 131, no. 16 (March 12, 2019): 5436–40. http://dx.doi.org/10.1002/ange.201901292.

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26

Shen, Bin, Wensheng Zhang, Jun Zhang, Jiankui Zhou, Jianying Wang, Li Chen, Lu Wang, et al. "Efficient genome modification by CRISPR-Cas9 nickase with minimal off-target effects." Nature Methods 11, no. 4 (March 2, 2014): 399–402. http://dx.doi.org/10.1038/nmeth.2857.

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27

Ling, Alexanda K., Clare C. So, Michael X. Le, Audrey Y. Chen, Lisa Hung, and Alberto Martin. "Double-stranded DNA break polarity skews repair pathway choice during intrachromosomal and interchromosomal recombination." Proceedings of the National Academy of Sciences 115, no. 11 (February 22, 2018): 2800–2805. http://dx.doi.org/10.1073/pnas.1720962115.

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Activation-induced cytidine deaminase (AID) inflicts DNA damage at Ig genes to initiate class switch recombination (CSR) and chromosomal translocations. However, the DNA lesions formed during these processes retain an element of randomness, and thus knowledge of the relationship between specific DNA lesions and AID-mediated processes remains incomplete. To identify necessary and sufficient DNA lesions in CSR, the Cas9 endonuclease and nickase variants were used to program DNA lesions at a greater degree of predictability than is achievable with conventional induction of CSR. Here we show that Cas9-mediated nicks separated by up to 250 nucleotides on opposite strands can mediate CSR. Staggered double-stranded breaks (DSBs) result in more end resection and junctional microhomology than blunt DSBs. Moreover, Myc-Igh chromosomal translocations, which are carried out primarily by alternative end joining (A-EJ), were preferentially induced by 5′ DSBs. These data indicate that DSBs with 5′ overhangs skew intrachromosomal and interchromosomal end-joining toward A-EJ. In addition to lending potential insight to AID-mediated phenomena, this work has broader carryover implications in DNA repair and lymphomagenesis.
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28

Nüesch, Jürg P. F., Romuald Corbau, Peter Tattersall, and Jean Rommelaere. "Biochemical Activities of Minute Virus of Mice Nonstructural Protein NS1 Are Modulated In Vitro by the Phosphorylation State of the Polypeptide." Journal of Virology 72, no. 10 (October 1, 1998): 8002–12. http://dx.doi.org/10.1128/jvi.72.10.8002-8012.1998.

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ABSTRACT NS1, the 83-kDa major nonstructural protein of minute virus of mice (MVM), is a multifunctional nuclear phosphoprotein which is required in a variety of steps during progeny virus production, early as well as late during infection. NS1 is the initiator protein for viral DNA replication. It binds specifically to target DNA motifs; has site-specific single-strand nickase, intrinsic ATPase, and helicase activities; trans regulates viral and cellular promoters; and exerts cytotoxic stress on the host cell. To investigate whether these multiple activities of NS1 depend on posttranslational modifications, in particular phosphorylation, we expressed His-tagged NS1 in HeLa cells by using recombinant vaccinia viruses, dephosphorylated it at serine and threonine residues with calf intestine alkaline phosphatase, and compared the biochemical activities of the purified un(der)phosphorylated (NS1O) and the native (NS1P) polypeptides. Biochemical analyses of replicative functions of NS1O revealed a severe reduction of intrinsic helicase activity and, to a minor extent, of ATPase and nickase activities, whereas its affinity for the target DNA sequence [ACCA]2–3 was enhanced compared to that of NS1P. In the presence of endogenous protein kinases found in replication extracts, NS1O showed all functions necessary for resolution and replication of the 3′ dimer bridge, indicating reactivation of NS1O by rephosphorylation. Partial reactivation of the helicase activity was found as well when NS1O was incubated with protein kinase C.
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29

Rysenkova, Karina D., Ekaterina V. Semina, Maxim N. Karagyaur, Anna A. Shmakova, Daniyar T. Dyikanov, Petr A. Vasiluev, Yury P. Rubtsov, Kseniya A. Rubina, and Vsevolod A. Tkachuk. "CRISPR/Cas9 nickase mediated targeting of urokinase receptor gene inhibits neuroblastoma cell proliferation." Oncotarget 9, no. 50 (June 29, 2018): 29414–30. http://dx.doi.org/10.18632/oncotarget.25647.

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30

Ishola, O. A., and K. T. h. e. v. a. Das. "22 Development of DOUBLE NICKASE CRISPR aganist latently infected human immunodeficency virus (HIV)." Journal of Virus Eradication 2 (July 2016): 16. http://dx.doi.org/10.1016/s2055-6640(20)30967-5.

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31

Li, Qi, François M. Seys, Nigel P. Minton, Junjie Yang, Yu Jiang, Weihong Jiang, and Sheng Yang. "CRISPR–Cas9 D10A nickase‐assisted base editing in the solvent producer Clostridium beijerinckii." Biotechnology and Bioengineering 116, no. 6 (February 21, 2019): 1475–83. http://dx.doi.org/10.1002/bit.26949.

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32

Aísa-Marín, Izarbe, M. José López-Iniesta, and Gemma Marfany. "Data on the generation of two Nr2e3 mouse models by CRISPR / Cas9D10A nickase." Data in Brief 33 (December 2020): 106447. http://dx.doi.org/10.1016/j.dib.2020.106447.

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33

Ge, Xi A., and Craig P. Hunter. "Efficient Homologous Recombination in Mice Using Long Single Stranded DNA and CRISPR Cas9 Nickase." G3: Genes|Genomes|Genetics 9, no. 1 (November 30, 2018): 281–86. http://dx.doi.org/10.1534/g3.118.200758.

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34

Iriki, Hoshie, Takefumi Kawata, and Tetsuya Muramoto. "Generation of deletions and precise point mutations in Dictyostelium discoideum using the CRISPR nickase." PLOS ONE 14, no. 10 (October 17, 2019): e0224128. http://dx.doi.org/10.1371/journal.pone.0224128.

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35

Sakuma, Tetsushi, Keiichi Masaki, Hiromi Abe-Chayama, Keiji Mochida, Takashi Yamamoto, and Kazuaki Chayama. "Highly multiplexed CRISPR-Cas9-nuclease and Cas9-nickase vectors for inactivation of hepatitis B virus." Genes to Cells 21, no. 11 (September 23, 2016): 1253–62. http://dx.doi.org/10.1111/gtc.12437.

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36

Tu, Jian, Zijun Huo, Mo Liu, Donghui Wang, An Xu, Ruoji Zhou, Dandan Zhu, et al. "Generation of human embryonic stem cell line with heterozygous RB1 deletion by CRIPSR/Cas9 nickase." Stem Cell Research 28 (April 2018): 29–32. http://dx.doi.org/10.1016/j.scr.2018.01.021.

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37

Chernukhin, V. A., J. Seggewiss, Yu G. Kashirina, D. A. Gonchar, and S. Kh Degtyarev. "Purification and properties of recombinant DNA methyltransferase M2.BstSE of the BstSEI nickase-modification system." Molecular Biology 43, no. 1 (February 2009): 8–15. http://dx.doi.org/10.1134/s0026893309010026.

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38

Nawaly, Hermanus, Yoshinori Tsuji, and Yusuke Matsuda. "Rapid and precise genome editing in a marine diatom, Thalassiosira pseudonana by Cas9 nickase (D10A)." Algal Research 47 (May 2020): 101855. http://dx.doi.org/10.1016/j.algal.2020.101855.

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39

Lunsford, R. Dwayne, Nga Nguyen, and J. London. "DNA-Binding Activities in Streptococcus gordonii : Identification of a Receptor-Nickase and a Histonelike Protein." Current Microbiology 32, no. 2 (February 1, 1996): 95–100. http://dx.doi.org/10.1007/s002849900017.

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40

Lee, Angus Yiu-fai, and Kevin C. Kent Lloyd. "Conditional targeting of Ispd using paired Cas9 nickase and a single DNA template in mice." FEBS Open Bio 4, no. 1 (January 1, 2014): 637–42. http://dx.doi.org/10.1016/j.fob.2014.06.007.

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41

Trafoier, T., S. Hainzl, T. Kocher, U. Koller, J. Reichelt, C. Heufler Tiefenthaler, and M. Schmuth. "159 CRISPR/Cas9 nickase mediated gene therapy in primary keratinocytes derived from patients with EPPK." Journal of Investigative Dermatology 141, no. 10 (October 2021): S175. http://dx.doi.org/10.1016/j.jid.2021.08.163.

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Lee, Jeong Hyo, Si Won Kim, and Tae Sub Park. "Myostatin gene knockout mediated by Cas9-D10A nickase in chicken DF1 cells without off-target effect." Asian-Australasian Journal of Animal Sciences 30, no. 5 (October 19, 2016): 743–48. http://dx.doi.org/10.5713/ajas.16.0695.

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Tewary, S. K., H. Zhao, W. Shen, J. Qiu, and L. Tang. "Structure of the NS1 Protein N-Terminal Origin Recognition/Nickase Domain from the Emerging Human Bocavirus." Journal of Virology 87, no. 21 (August 21, 2013): 11487–93. http://dx.doi.org/10.1128/jvi.01770-13.

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Wu, Yong, Tieli Gao, Xiaolin Wang, Youjin Hu, Xuyun Hu, Zhiqing Hu, Jialun Pang, et al. "TALE nickase mediates high efficient targeted transgene integration at the human multi-copy ribosomal DNA locus." Biochemical and Biophysical Research Communications 446, no. 1 (March 2014): 261–66. http://dx.doi.org/10.1016/j.bbrc.2014.02.099.

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Zhao, Guannan, Qinghui Wang, Qingqing Gu, Wenan Qiang, Jian-Jun Wei, Peixin Dong, Hidemichi Watari, Wei Li, and Junming Yue. "Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells." Oncotarget 8, no. 55 (October 17, 2017): 94666–80. http://dx.doi.org/10.18632/oncotarget.21863.

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Choi, Ji-Young, Chulman Jo, and Sangmee Ahn Jo. "Construction of a new T-vector: Nickase (Nt.BspQI)-generated T-vector bearing a reddish-orange indicator gene." Tissue Engineering and Regenerative Medicine 13, no. 1 (February 2016): 66–69. http://dx.doi.org/10.1007/s13770-015-0118-z.

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Rogulin, E. A., T. A. Perevyazova, L. A. Zheleznaya, and N. I. Matvienko. "Plasmid pRARE as a Vector for Cloning to Construct a Superproducer of the Site-Specific Nickase N.BspD6I." Biochemistry (Moscow) 69, no. 10 (October 2004): 1123–27. http://dx.doi.org/10.1023/b:biry.0000046886.19428.d5.

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Wang, Luying, Xingying Shen, Ting Wang, Pinru Chen, Nan Qi, Bin-Cheng Yin, and Bang-Ce Ye. "A lateral flow strip combined with Cas9 nickase-triggered amplification reaction for dual food-borne pathogen detection." Biosensors and Bioelectronics 165 (October 2020): 112364. http://dx.doi.org/10.1016/j.bios.2020.112364.

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Rong, Zhili, Shengyun Zhu, Yang Xu, and Xuemei Fu. "Homologous recombination in human embryonic stem cells using CRISPR/Cas9 nickase and a long DNA donor template." Protein & Cell 5, no. 4 (March 14, 2014): 258–60. http://dx.doi.org/10.1007/s13238-014-0032-5.

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Naeem, Muhammad, Saman Majeed, Mubasher Zahir Hoque, and Irshad Ahmad. "Latest Developed Strategies to Minimize the Off-Target Effects in CRISPR-Cas-Mediated Genome Editing." Cells 9, no. 7 (July 2, 2020): 1608. http://dx.doi.org/10.3390/cells9071608.

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Abstract:
Gene editing that makes target gene modification in the genome by deletion or addition has revolutionized the era of biomedicine. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 emerged as a substantial tool due to its simplicity in use, less cost and extraordinary efficiency than the conventional gene-editing tools, including zinc finger nucleases (ZFNs) and Transcription activator-like effector nucleases (TALENs). However, potential off-target activities are crucial shortcomings in the CRISPR system. Numerous types of approaches have been developed to reduce off-target effects. Here, we review several latest approaches to reduce the off-target effects, including biased or unbiased off-target detection, cytosine or adenine base editors, prime editing, dCas9, Cas9 paired nickase, ribonucleoprotein (RNP) delivery and truncated gRNAs. This review article provides extensive information to cautiously interpret off-target effects to assist the basic and clinical applications in biomedicine.
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