Search results for "CRISPR-Associated Protein 9"

showing 2 items of 2 documents

CRISPR-mediated strand displacement logic circuits with toehold-free DNA

2021

DNA nanotechnology, and DNA computing in particular, has grown extensively over the past decade to end with a variety of functional stable structures and dynamic circuits. However, the use as designer elements of regular DNA pieces, perfectly complementary double strands, has remained elusive. Here, we report the exploitation of CRISPR-Cas systems to engineer logic circuits based on isothermal strand displacement that perform with toehold-free double-stranded DNA. We designed and implemented molecular converters for signal detection and amplification, showing good interoperability between enzymatic and nonenzymatic processes. Overall, these results contribute to enlarge the repertoire of su…

0106 biological sciencesLetterTranscription GeneticComputer scienceStreptococcus pyogenesRibonuclease HBiomedical EngineeringDNA Single-StrandedNanotechnology01 natural sciencesBiochemistry Genetics and Molecular Biology (miscellaneous)Displacement (vector)law.invention03 medical and health sciencesSynthetic biologychemistry.chemical_compoundComputers MolecularDNA computinglaw010608 biotechnologyCRISPR-Associated Protein 9Biological computingDNA nanotechnologyCRISPRNanotechnologyClustered Regularly Interspaced Short Palindromic RepeatsGene Regulatory NetworksDNA nanotechnologySynthetic biology030304 developmental biologyElectronic circuit0303 health sciencesGeneral MedicineRibonuclease PancreaticchemistryLogic gatebiological computingsynthetic biologyCRISPR-Cas SystemsEndopeptidase KGenetic EngineeringDNARNA Guide Kinetoplastida
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Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
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