The largest database of trusted experimental protocols
> Physiology > Genetic Function > DNA Repair

DNA Repair

DNA repair is a crucial cellular process that maintains the integrity of genetic information by identifying and correcting various types of DNA damage, such as single-strand breaks, double-strand breaks, and base modifications.
This process involves a complex network of enzymes, signaling pathways, and repair mechanisms that work together to restore the original DNA sequence and prevent the accumulation of mutations.
Deficiencies in DNA repair can lead to genetic instability, increased susceptibility to cancer, and other human diseases.
Researchers in the field of DNA repair utilize a variety of experimental techniques and protocols to study these processes, including gene expression analysis, DNA damage assays, and the development of novel therapeutic interventions.
The PubCompare.ai tool can help scientists in this field streamline their research by providing AI-driven optimizarion of DNA repair protocols, allowing them to easily identify the most effective and reproducible methods from the scientific literature, preprints, and patents.

Most cited protocols related to «DNA Repair»

We have developed a protocol that builds on the RADseq method [19] (link) but which differs in two principal respects (Figure 2). First, our method eliminates random shearing and end repair of genomic DNA (an advantage shared with a family of partially overlapping protocols such as MSG, CrOPS, and other recent RADseq derivatives [9] , [20] (link), [21] (link)). Instead, we use a double restriction enzyme (RE) digest (i.e., a restriction digest with two enzymes simultaneously) that results in at least five-fold reduction in library production cost–complete ddRADseq libraries cost ∼$5 per sample, while the necessary enzymatic steps following the initial restriction digest and ligation in random shearing RAD libraries alone introduce a cost of ∼$25 per library (NEB, Ipswich, MA). Furthermore, the elimination of several high-DNA-loss steps permits construction of ddRAD libraries from 100 ng or less of starting DNA. Second, we introduced a precise selection for genomic fragments by size, which allows greater fine-scale control of the fraction of regions represented in the final library (see results). By combining precise and repeatable size selection with sequence-specific fragmentation, double digest Restriction-Site Associated DNA sequencing (ddRADseq) produces sequencing libraries consisting of only the subset of genomic restriction digest fragments generated by cuts with both REs (i.e., have one end from each cut) and which fall within the size-selection window (Figure 2B). This combination of requirements can be tuned to generate libraries consisting of fragments derived from hundreds to hundreds of thousands of regions genome-wide.
Precise, repeatable size selection offers two further advantages. First, because only a small fraction of restriction fragments will fall in the target size-selection regime (<5% in conditions described here), the probability of sampling both directions from the same restriction site is low. This reduces “duplicate” (i.e., immediately neighboring) region sampling, which effectively halves the number of reads that are required to reach high-confidence sampling of a SNP associated with a given RE cut site. Second, shared bias in region representation favoring fragments closest to the mean of size selection, in turn, biases independent samples (e.g., from different individuals) towards recovering the same genomic regions (Figure 2B). Because of this correlated recovery, regions are “filled in” with reads in approximately the same order across all individual samples, and samples with read recovery counts below saturation will still share a significant number of well-covered regions (“Experimental ddRADseq results” below; Analysis S1 Supporting Figure 4; Analysis S1 “Region recovery: ddRADseq vs. random shearing”). Both of these properties make the ddRADseq method robust to under-sampling with respect to read counts, which is a commonly observed problem arising from unequal read representation across individual samples in pooled sequencing experiments [9] , [22] (link), [23] .
Publication 2012
Crop, Avian derivatives DNA Library DNA Repair DNA Restriction Enzymes Enzymes Genome Ligation

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2018
Diploid Cell DNA Repair Gene Deletion Gene Silencing Homologous Recombination Malignant Neoplasms Mutation TP53 protein, human
After reviewing almost all cancer single-cell sequencing studies, we concluded 14 crucial functional states of cancer cells, including stemness, invasion, metastasis, proliferation, EMT, angiogenesis, apoptosis, cell cycle, differentiation, DNA damage, DNA repair, hypoxia, inflammation and quiescence. To characterize these functional states for cancer single cells, we built the corresponding gene signatures through searching literatures and known databases (including some general databases, such as Gene Ontology (17 (link)) and MSigDB (18 (link)), and some specialized databases, such as Cyclebase (19 (link)), HCMDB (20 (link)) and StemMapper (21 (link))) (Supplementary Table S2). For most of the signatures, the collected genes that were mentioned in more than two resources were kept. While for the invasion signature, genes mentioned in more than two invasion-associated terms collected from MSigDB were retained. Then, through functional annotations and literature searching, genes that negatively affect the corresponding functional states were removed.
Based on these signatures, the activities of 14 functional states across cancer single cells in each dataset were evaluated using Gene Set Variation Analysis (GSVA) with the GSVA package in R (22 (link)). In brief, for each gene, we first performed a non-parametric kernel estimation of its cumulative density function and then calculated an expression-level statistic to normalize expression profiles to a common scale. The expression-level statistic can reflect whether a gene is highly or lowly expressed in a specific cell in the context of the cell population distribution. Then, in each cell, the expression-level statistics of all genes were converted to normalized ranks. Next, we used the Kolmogorov–Smirnov like random walk statistic, similar to the GSEA method, to summarize the expression-level rank statistics of a given signature gene set into a final enrichment score (i.e. GSVA score), which is used to characterize the signature activity. At last, the enrichment scores of 14 signatures across cells in all scRNA-seq data were calculated. Then, for each single-cell dataset derived from tumor tissue, PDX and CTC, we identified significant correlations between gene expressions and functional state activities using Spearman's rank correlation test with Benjamini & Hochberg false discovery rate (FDR) correction for multiple comparisons (correlation > 0.3 and FDR < 0.05). Due to the low amount of mRNA within individual cells and sequencing technical noise, there is an excessive number of zeros in scRNA-seq data. During the calculation of gene-state associations, only cells with detectable expression of the genes of interest were used by setting the parameter ‘na.action’ to na.omit, and at least 30 cancer single cells were required.
Publication 2018
angiogen Apoptosis Cell Cycle Cells DNA Damage DNA Repair Gene Expression Genes Genetic Diversity Hypoxia Inflammation Malignant Neoplasms Neoplasm Metastasis Neoplasms RNA, Messenger Single-Cell RNA-Seq Tissues
Alignment and tree inference methods are often validated by simulating sequence evolution in silico. I chose not to do so in this work. Simulations employ drastically simplified models of evolution which are similar to the drastically simplified models used by multiple alignment and tree inference algorithms. In reality, sequence evolution is an enormously complex process disrupted by historical contingencies ranging from fortuitous outcomes of DNA repair machinery failures and narrowly-won host-pathogen arms races to asteroid impacts. Therefore, simulations of deep evolutionary history are at best suggestive and at worst entirely uninformative if one is interested in real biology. Simulations also exacerbate a common sociological problem in computational biology, namely that the developers of a new method have an opportunity to fish for significance before publication. Confronted with disappointing results, authors may rationalise tweaking a simulation until improved (simulated) performance is obtained for their method. These considerations beg the question of whether simulations could convincingly support the main claims of this paper, which are (1) Muscle5 MSA replicates have high and practically indistinguishable accuracy, and (2) the effects of alignment errors can be assessed by comparing inferences from different replicates. Claim (1) is supported by results on structure-based benchmarks. While structural similarity does not necessarily imply sequence homology, structural alignments are largely independent of sequence, and greater agreement with structural alignments therefore surely correlates strongly with more accurate alignment of homologous residues. If a simulation fails to recapitulate relative algorithm performance according to structure, the failure is more plausibly explained by a defect in the simulation than a defect in the structural benchmark. Claim (2) is self-evidently true because two different alignments of the same sequences cannot both be correct.
Publication 2022
Arm, Upper Biological Evolution DNA Repair Fishes Pathogenicity Sequence Alignment Trees

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2012
Buffers Cells Centrifugation Chromatin Cold Temperature DNA Chips DNA Library DNA Repair Endopeptidase K Enzymes Ethanol Formaldehyde Freezing G-substrate Glycine Immobilization Immunoglobulins Ligation Nitrogen Pellets, Drug Protease Inhibitors Radioimmunoprecipitation Assay Sodium Chloride

Most recents protocols related to «DNA Repair»

The database cancer single-cell state atlas (SEA) (http://biocc.hrbmu.edu.cn/CancerSEA/) was created to examine distinct functional states at the single cell level, and contains data on 14 functional states, including metastasis, invasion, apoptosis, cell cycle, differentiation, DNA damage, DNA repair, inflammation, and DNA damage.[19 ] We investigated the distribution and associated functions of complement C1q A chain (C1qA), complement C1q B chain (C1qB), and complement C1q C chain (C1qC) in SKCM using the Cancer SEA database.
Publication 2023
Apoptosis Cell Cycle Cells Complement C1q Complement Factor B DNA Damage DNA Repair Inflammation Malignant Neoplasms Neoplasm Metastasis
The normalized gene expression data for 266 breast cancer (BRCA) patients were downloaded from Table S7 in [29 (link)]. Gene expression profiles for 2,204 genes involved in either DNA metabolic or immune response processes of the Gene Ontology (GO) database were selected for the analysis.
For mutational signatures, somatic mutation data were downloaded from the ICGC data portal [30 ]. The 3,479,652 point mutations were assigned to mutational signatures using SigMa [9 (link)]. SigMa divided all mutations into two groups, close-by Clustered and Dispersed mutations, and assigned each of these mutations to one of 12 COSMIC v2 signatures [31 ] which were previously identified as active in BRCA (Signatures 1, 2, 3, 5, 6, 8, 13, 17, 18, 20, 26, and 30). From the signatures classified by SigMa as described above, signature phenotype profiles 1D, 2C/D, 3C/D, 5D, 8C/D, and 13C/D that had exposure levels of at least 10% within each group were selected for further analysis (the numbering refers to the COSMIC signature index and C/D denotes signatures attributed to clustered and dispersed mutations). Examining their correlation patterns among patients, some of the signatures were grouped as follows: Signatures 3C/D and 8D were combined into DSB (double-stranded DNA break repair) related signatures, and Signatures 2C and 13C/D into APOBEC related signatures. The remaining signatures are treated separately, resulting in Signature 1, 2D, 5, APOBEC, DSB. A log transformation was consequently performed on exposures of each signature to make its distribution shape closer to a bell curve of normality.
Furthermore, we included binary information of homologous recombination deficiency as an additional variable in the analysis. The binary alteration information was obtained by aggregating functional inactivation information for BRCA1/BRCA2 and 16 other HR genes as provided in Supplementary Tables 4a and 4b of Davies et al. [32 (link)]. The positive entries were assigned a real value of 4.218 in the SPCS model with the hyperparameter search for the best performance in terms of the means of minimum least square errors and maximum Pearson correlation between responses and predictions over all nodes.
Publication 2023
A 218 BRCA1 protein, human Cosmic composite resin Diploid Cell DNA Repair Gene, BRCA2 Gene Expression Genes Homologous Recombination Malignant Neoplasm of Breast Mutation Patients Phenotype Point Mutation Response, Immune

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2023
Apoptosis Biological Processes Cellular Structures DNA Repair DNA Replication Neoplastic Cell Transformation Operator, Genetic Signal Transduction Pathways
We used KAPA Hyper Prep Kits (Kapa Biosystems, Wilmington, MA) to create barcoded paired-end libraries with 300-bp inserts and hybridized the barcoded samples to a custom NimbleGen SeqCap (Roche, Basel, Switzerland) or SureSelectXT (Agilent, Santa Clara, CA) targeted-gene capture kit. We used custom bait designs which included 577 candidate cancer susceptibility genes involved in the response to DNA damage, DNA repair, cell cycle regulation, programmed cell death, and PI3K/AKT/mTOR pathways (Supplemental Table 2). Following capture, samples were sequenced with 2 × 100 bp paired end reads on a GAIIx or HiSeq 2500 (Illumina, San Diego, CA) in the COH Integrative Genomics Core (IGC) with germline samples sequenced to an average coverage of 84.1-fold and tumor samples sequenced to an average coverage of 84.5-fold. Paired-end reads from each sample were aligned to human reference genome (GRCh37/hg19) using the Burrows-Wheeler Alignment Tool (BWA, v0.7.5a-r405) under default settings(47 (link)), and the aligned binary alignment map (BAM) sequence files were sorted and indexed using SAMtools (v0.1.19) (48 (link)). The sorted and indexed BAM files were processed by Picard MarkDuplicates (v1.105, http://picard.sourceforge.net/) to remove duplicate sequencing reads. A pileup file was then created via mpileup in SAMtools (48 (link)) and germline and somatic variants were called using Varscan2 (v.2.2.8) (49 (link)). These variants were subsequently annotated using ANNOVAR (50 ).
Publication Preprint 2023
Apoptosis BP 100 Cell Cycle Control Diploid Cell DNA Damage DNA Repair FRAP1 protein, human Gene, Cancer Genes Genome, Human Germ Line Neoplasms PIK3CB protein, human Susceptibility, Disease
A plasmid encoding human IP3R3 was obtained from Harvard PlasmID Database (Clone ID: HsCD00399229, GenBank Accession: BC172406) and cloned from pENTR223 into pcDNA3.2/V5-DEST using LR Gateway cloning. We tagged human IP3R3 with a SNAP-tag, a self-labeling enzyme tag based on the human DNA repair protein, O6-alkylguanine-DNA-alkyltransferase, which reacts with O6-benzylguanine derivatives conjugated to fluorescent dyes (32 (link)). To generate the N-terminally SNAP-tagged human IP3R3 construct (SNAP-IP3R3), PCR was used to amplify an IP3R3 fragment (forward primer: CTCGGCGGTGGTTCTGGTGGTGGTTCTGGTATGAGTGAAATGTCCAGC, reverse primer: GAACCGCGGGCCCTCTAGATCAACCACTTTTGTACAAGAAAGCTGGGC), and BsrGI restriction digest was used to generate a backbone fragment. Gibson assembly was used to introduce a DNA string (GeneArt Strings, Thermo Fisher Scientific) encoding SNAPf (fast-labeling SNAP-tag) with a GGSGGGSG peptide linker between the backbone fragment and the IP3R3 fragment (Fig. 1A). For expression of SNAP-IP3R3 under control of a tetracycline-inducible promoter, SNAP-IP3R3 was transferred from pcDNA3.2 to pDONR221 and then to pT-REx-DEST30 using BP and LR Gateway cloning, respectively.
To generate the construct encoding IP3R3 with reduced affinity for IP3 (SNAP-IP3R3RQ, Fig. 6A), a DNA string was synthesized encoding a region of SNAP-IP3R3 between two restriction sites, BsiWI and RsrII, which contained an Arg to Gln mutation at residue 568 (R568Q, CGC to CAG). A BsiWI/RsrII-restriction digest of SNAP-IP3R3 in pDONR221 was used to generate a fragment encoding the remainder of the construct. Gibson assembly was used to assemble the two fragments, and SNAP-IP3R3RQ was transferred to pT-REx-DEST30 using LR Gateway cloning. Sequences of all coding regions were confirmed using Sanger sequencing (Source BioScience). A silent point mutation was detected in bases (ATC to ATA) encoding Ile2512 in both constructs.
Publication 2023
3-((2-nitro-4-azidophenyl)-2-aminoethyldithio)-N-succinimidyl propionate arginyl-glutamine BPIFA4P protein, human derivatives DNA, A-Form DNA Repair Enzymes Exons Fluorescent Dyes Homo sapiens MGMT protein, human Mutation O(6)-benzylguanine Oligonucleotide Primers Peptide Fragments Plasmids Silent Mutation Tetracycline Vertebral Column

Top products related to «DNA Repair»

Sourced in United States, United Kingdom
The NEBNext FFPE DNA Repair Mix is a reagent designed to repair DNA damage in samples that have been formalin-fixed and paraffin-embedded (FFPE). The mix contains enzymes and buffers that help to restore the integrity of DNA molecules extracted from FFPE tissues, enabling their use in downstream molecular biology applications.
Sourced in United States, United Kingdom, Germany, Canada, France, Australia, China, Japan, Italy, Switzerland, Netherlands
AMPure XP beads are a magnetic bead-based product used for the purification of nucleic acids, such as DNA and RNA, from various samples. The beads are designed to selectively bind to nucleic acids, allowing for the removal of contaminants and unwanted molecules during the purification process. The core function of AMPure XP beads is to provide an efficient and reliable method for the cleanup and concentration of nucleic acids in preparation for downstream applications.
Sourced in United States
The End-It DNA End-Repair Kit is a laboratory tool designed to perform end-repair on DNA fragments. It enables the conversion of various DNA end structures, such as 3' overhangs, 5' overhangs, and blunt ends, into blunt ended DNA fragments. This process prepares the DNA for further downstream applications.
Sourced in United States, United Kingdom
The G-TUBE is a sample preparation device designed for efficient genomic DNA extraction from a wide range of sample types. It utilizes Covaris' proprietary acoustic technology to gently and effectively lyse cells and tissues, releasing high-quality genomic DNA for downstream applications.
Sourced in United States, United Kingdom
The NEBNext Ultra II End Repair/dA-Tailing Module is a reagent kit designed to perform end repair and dA-tailing of DNA fragments in preparation for next-generation sequencing library construction. The module contains the necessary enzymes and buffers to convert DNA fragments with various end structures into a uniform population with 3' dA-overhangs, which is a required step for subsequent adapter ligation.
Sourced in United States, Germany, Canada, United Kingdom, France, China, Japan, Spain, Ireland, Switzerland, Singapore, Italy, Australia, Belgium, Denmark, Hong Kong, Netherlands, India
The 2100 Bioanalyzer is a lab equipment product from Agilent Technologies. It is a microfluidic platform designed for the analysis of DNA, RNA, and proteins. The 2100 Bioanalyzer utilizes a lab-on-a-chip technology to perform automated electrophoretic separations and detection.
Sourced in United States, China, Germany, United Kingdom, Hong Kong, Canada, Switzerland, Australia, France, Japan, Italy, Sweden, Denmark, Cameroon, Spain, India, Netherlands, Belgium, Norway, Singapore, Brazil
The HiSeq 2000 is a high-throughput DNA sequencing system designed by Illumina. It utilizes sequencing-by-synthesis technology to generate large volumes of sequence data. The HiSeq 2000 is capable of producing up to 600 gigabases of sequence data per run.
Sourced in United States, China, Germany, United Kingdom, Canada, Japan, France, Italy, Switzerland, Australia, Spain, Belgium, Denmark, Singapore, India, Netherlands, Sweden, New Zealand, Portugal, Poland, Israel, Lithuania, Hong Kong, Argentina, Ireland, Austria, Czechia, Cameroon, Taiwan, Province of China, Morocco
Lipofectamine 2000 is a cationic lipid-based transfection reagent designed for efficient and reliable delivery of nucleic acids, such as plasmid DNA and small interfering RNA (siRNA), into a wide range of eukaryotic cell types. It facilitates the formation of complexes between the nucleic acid and the lipid components, which can then be introduced into cells to enable gene expression or gene silencing studies.
Sourced in United States, Germany, Canada, China, France, United Kingdom, Japan, Netherlands, Italy, Spain, Australia, Belgium, Denmark, Switzerland, Singapore, Sweden, Ireland, Lithuania, Austria, Poland, Morocco, Hong Kong, India
The Agilent 2100 Bioanalyzer is a lab instrument that provides automated analysis of DNA, RNA, and protein samples. It uses microfluidic technology to separate and detect these biomolecules with high sensitivity and resolution.
Sourced in United States, China, United Kingdom, Germany, Japan, France, Canada, Morocco, Switzerland, Australia
T4 DNA ligase is an enzyme that catalyzes the formation of phosphodiester bonds between adjacent 3'-hydroxyl and 5'-phosphate termini in DNA. It is commonly used in molecular biology for the joining of DNA fragments.

More about "DNA Repair"

DNA repair is a critical cellular process that maintains the integrity of genetic information by identifying and correcting various types of DNA damage, such as single-strand breaks, double-strand breaks, and base modifications.
This process involves a complex network of enzymes, signaling pathways, and repair mechanisms that work together to restore the original DNA sequence and prevent the accumulation of mutations.
Deficiencies in DNA repair can lead to genetic instability, increased susceptibility to cancer, and other human diseases.
Researchers in the field of DNA repair utilize a variety of experimental techniques and protocols to study these processes, including gene expression analysis, DNA damage assays, and the development of novel therapeutic interventions.
Some key tools and products used in DNA repair research include the NEBNext FFPE DNA Repair Mix, which repairs damaged DNA from formalin-fixed, paraffin-embedded (FFPE) samples, and the AMPure XP beads, which can be used for DNA purification and size selection.
The End-It DNA End-Repair Kit and the NEBNext Ultra II End Repair/dA-Tailing Module are also commonly used to prepare DNA samples for sequencing, ensuring that the ends are properly repaired and compatible with downstream applications.
The G-TUBE can be used to mechanically fragment DNA, while the 2100 Bioanalyzer and HiSeq 2000 are high-throughput sequencing platforms that enable researchers to analyze DNA repair processes at a genomic scale.
Lipofectamine 2000 is a transfection reagent that can be used to introduce genetic material, such as DNA repair genes or reporter constructs, into cells to study their function.
The Agilent 2100 Bioanalyzer is another useful tool for analyzing DNA samples, providing information on size, concentration, and quality.
Finally, T4 DNA ligase is a essential enzyme used in DNA repair and recombination, as it can join the ends of DNA fragments together, enabling the restoration of the original DNA sequence.
By leveraging these tools and techniques, researchers in the field of DNA repair can gain valuable insights into the mechanisms and regulation of this crucial cellular process, paving the way for the development of new diagnostic and therapeutic interventions for genetic diseases and cancer.