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> Disorders > Cell or Molecular Dysfunction > DNA Damage

DNA Damage

DNA damage is a critical cellular event that can lead to genetic instability and disease.
It can be caused by various endogenous and exogenous factors, including reactive oxygen species, ultraviolet radiation, and chemical agents.
Efficient and accurate detection and quantification of DNA damage is essential for understanding its underlying mechanisms and developing effective interventions.
PubCompare.ai helps researchers optimize their DNA damage research protocols for reproducibility and accuracy by locating the best protocols from literature, pre-prints, and patents using AI-driven comparisons and analysis.
This streamlines the research process and ensures accurate, reliable results.

Most cited protocols related to «DNA Damage»

1
Modeling DNA Damage Misincorporations
The general idea is to mutate bases following an Hasegawa, Kishino and Yano (HKY) transition matrix (Hasegawa et al., 1985 (link)) and then independently add post-mortem damage on top of mutated bases. In this framework, we have multinomial distributions describing the position-specific substitutions for any given base ( and ).

Θ is the HKY transition matrix, and is defined as the DNA damage transition matrix. We assume post-mortem cytosine deamination is the main driver of nucleotide misincorporations in agreement with experimental evidence (Briggs et al., 2007 (link)), providing

Where the base-specific damage probabilities are defined as

The motivation for the base-specific damage probabilities is best explained by the Markov chain in Figure 1 where the first jump decides if the position is before or after a nick; then a substitution could be observed following deamination in overhang or double-stranded DNA regions. A similar Markov chain could be drawn for substitutions (Supplementary Section 1).

A schematic view describing the DNA damage Markov chain, which extends the DNA substitution model. The states and correspond to the final nucleotides in the sequences

For rescaling base quality scores, we assume that and substitutions either originate from true biological differences or from damage driven misincorporations. We can derive an estimate for the probability that a (similar for ) misincorporation at position i along the reads is due to damage using

We can now correct base quality scores provided in alignment BAM files [ at position i for read r] using

Jónsson H., Ginolhac A., Schubert M., Johnson P.L, & Orlando L. (2013). mapDamage2.0: fast approximate Bayesian estimates of ancient DNA damage parameters. Bioinformatics, 29(13), 1682-1684.
Publication 2013
Autopsy Biopharmaceuticals Cytosine Deamination DNA, Double-Stranded DNA Damage Motivation Nucleotides
2
Characterizing Cancer Cell Functional States via scRNA-seq
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.
Yuan H., Yan M., Zhang G., Liu W., Deng C., Liao G., Xu L., Luo T., Yan H., Long Z., Shi A., Zhao T., Xiao Y, & Li X. (2018). CancerSEA: a cancer single-cell state atlas. Nucleic Acids Research, 47(Database issue), D900-D908.
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
3
Automated Comet Assay Image Analysis

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Publication 2014
Cells Comet Assay DNA Damage Epistropheus Head Light Olea europaea Tail
4
Automated Comet Assay Image Analysis

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Publication 2014
1,1'-((4,4,7,7-tetramethyl)-4,7-diazaundecamethylene)bis-4-(3-methyl-2,3-dihydro(benzo-1,3-oxazole)-2-methylidine)quinolinium, tetraiodide Cells Comet Assay DAPI DNA Damage EDNRB protein, human Fluorescent Dyes Gold Head Light Propidium Iodide Silver Nitrate SYBR Green I Tail
5
CtIP-Mediated DNA Damage Response
HeLa, HCC1937, U2OS and U2OS-derived cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% foetal bovine serum (FBS) and standard antibiotics. Data for survival curves were generated by colony formation assays. In brief, U2OS cells were transfected with siRNA (see Supplementary Methods) and treated with DNA-damage-inducing drugs. After 1 h, the drug was removed and cells were left for 10-14 days at 37°C to allow colonies to form. Colonies were stained with 0.5% crystal violet/20% ethanol and counted. Where indicated, cells were pre-incubated with aphidicolin (10 μM) for 90 min, then treated with the specified drug and aphidicolin for 1 h. A U2OS-derived cell line stably expressing GFP-ATR was described previously7 (link). The siRNA-resistant silent wild-type GFP-CtIP construct was generated by sub-cloning the CtIP cDNA into the pEGFP-C1 expression plasmid (BD Biosciences Clontech) and changing three nucleotides in the CtIP-1 siRNA targeting region by using a QuikChange site-directed mutagenesis kit (Stratagene, Inc.) as previously described16 (link). The plasmid expressing the CtIP mutant lacking the C-terminus (1-789) was generated by changing residues 790 and 791 in the wild-type GFP-CtIP construct to two stop-codons. For generation of cell lines stably expressing siRNA-resistant GFP-tagged wild-type and mutant CtIP, U2OS cells were transfected with the appropriate constructs and, following antibiotic selection, resistant clones were tested for expression and nuclear localization of the transgene-product by immunofluorescence microscopy. To detect ssDNA by microscopy, cells were cultivated for 24 h in medium supplemented with 10 μM BrdU prior to camptothecin treatment and, after fixation, immunostained with an anti-BrdU antibody (see Methods) without any preceding DNA denaturation or nuclease treatment48 (link). Laser micro-irradiation was performed as described previously30 (link),31 (link). Recombinant FLAG-GST-CtIP-6H was isolated from baculovirus-infected Sf9 cells as described previously49 (link). Recombinant MRE11-RAD50 (MR) and MRE11-RAD50-NBS1 (MRN) complex were kind gifts from T. Paull.
Full Methods and any associated references are available in the online version of the paper at www.nature.com/nature.
Sartori A.A., Lukas C., Coates J., Mistrik M., Fu S., Bartek J., Baer R., Lukas J, & Jackson S.P. (2007). Human CtIP promotes DNA end resection. Nature, 450(7169), 509-514.
Publication 2007
Antibiotics Antibodies, Anti-Idiotypic Aphidicolin Baculoviridae Biological Assay Bromodeoxyuridine Camptothecin Cell Lines Cells Clone Cells Codon, Terminator DNA, Complementary DNA, Single-Stranded DNA Damage DNA Denaturation Eagle Ethanol Fetal Bovine Serum Gifts HeLa Cells Immunofluorescence Microscopy Microscopy Mutagenesis, Site-Directed Nucleotides Pharmaceutical Preparations Plasmids Rad50 protein, human Radiotherapy RBBP8 protein, human RNA, Small Interfering Sf9 Cells Transgenes Violet, Gentian

Most recents protocols related to «DNA Damage»

1
Targeting ADAR1 in High Interferon Tumors
Not available on PMC !

Example 17

Since interferon signaling is spontaneously activated in a subset of cancer cells and exposes potential therapeutic vulnerabilities, it was tested whether there is evidence for similar endogenous interferon activation in primary human tumors. An IFN-GES threshold was computed to predict ADAR dependency across the CCLE cell lines and was determined to be a z-score above 2.26 (FIG. 66, panel A). This threshold was applied to The Cancer Genome Atlas (TCGA) tumors, to identify primary cancers with similarly high interferon activation. Restricting the analysis to the 4,072 samples analyzed by TCGA with at least 70% tumor purity as estimated by the ABSOLUTE algorithm (Carter et al. (2012) Nat. Biotechnol. 30:413-421), 2.7% of TCGA tumors displayed IFN-GESs above this threshold (FIG. 66, panel B and. GSEA of amplified genes in these high purity, high interferon tumors revealed the top pathway as “Type I Interferon Receptor Binding”, comprising 17 genes that all encode type I interferons and are clustered on chromosome 9p21.3 (FIG. 67).

Furthermore, analysis of TCGA copy number data showed that the interferon gene cluster including IFN-β (IFNβI), IFN-ε (IFNE), IFN-ω (IFNWI), and all 13 subtypes of IFN-α on chromosome 9p21.3, proximal to the CDKN2A/CDKN2B tumor suppressor locus, is one of the most frequently homozygously deleted regions in the cancer genome. The interferon genes comprise 16 of the 26 most frequently deleted coding genes across 9,853 TCGA cancer specimens for which ABSOLUTE copy number data are available (FIG. 66, panels C and D). Interferon signaling and activation, both in tumors with high IFN-GESs or deletions in chromosome 9p, therefore represent a biomarker to stratify patients who benefit from interferon modulating therapies.

In summary, specific cancer cell lines have been identified with elevated IFN-β signaling triggered by an activated cytosolic DNA sensing pathway, conferring dependence on the RNA editing enzyme, ADAR1. In cells with low, basal interferon signaling, the cGAS-STING pathway is inactive and PKR levels are reduced (FIG. 68, panel A). Upon cGAS-STING activation, interferon signaling and PKR protein levels are elevated but ADAR1 is still able to suppress PKR activation (FIG. 68, panel B). However, once ADAR1 is deleted, the abundant PKR becomes activated and leads to downstream signaling and cell death (FIG. 68, panel C). This is also shown in normal cells lines (e.g. A549 and NCI-H1437) once exogenous interferon is introduced (FIG. 68, panel D). ADAR1 deficiency in cell lines with high interferon levels, whether from endogenous or exogenous sources, led to phosphorylation and activation of PKR, ATF4-mediated gene expression, and apoptosis. Recent studies have shown that cGAS activation and innate interferon signaling, induced by cytosolic DNA released from the nucleus by DNA damage and genome instability (Mackenzie et al. (2017) Nature 548:461-465; Harding et al. (2017) Nature 548:466-470), led to elevated interferon-related gene expression signatures, which have been linked to resistance to DNA damage, chemotherapy, and radiation in cancer cells (Weichselbaum et al. (2008) Proc. Natl. Acad. Sci. USA 105:18490-18495). In high-interferon tumors, blocking ADAR1 might be effective to induce PKR-mediated apoptotic pathways while upregulating type I interferon signaling, which could contribute to anti-tumor immune responses (Parker et al. (2016) Nature 16:131-144). Alternatively, in tumors without activated interferon signaling, ADAR1 inhibition can be combined with localized interferon inducers, such as STING agonists, chemotherapy, or radiation. Generation of specific small molecule inhibitors targeting ADAR1 exploits this novel vulnerability in lung and other cancers and serves to enhance innate immunity in combination with immune checkpoint inhibitors.

US11873486B2. Modulating dsRNA editing, sensing, and metabolism to increase tumor immunity and improve the efficacy of cancer immunotherapy and/or modulators of intratumoral interferon (2024-01-16). Dana-Farber Cancer Institute, Inc. [US]. Inventors: Matthew Meyerson [US], William N. Haining [US], Jeffrey Ishizuka [US], Robert Manguso [US], Hugh Gannon [US].
Patent 2024
agonists Apoptosis ATF4 protein, human Biological Markers CDKN2A Gene Cell Death Cell Lines Cell Nucleus Cells Chromogranin A Chromosome Deletion Chromosomes, Human, Pair 3 Cytosol DNA Damage Electromagnetic Radiation Enzymes Gene, Cancer Gene Clusters Gene Expression Genes Genome Genomic Instability Homo sapiens IFNAR2 protein, human Immune Checkpoint Inhibitors Immunity, Innate inhibitors Interferon-alpha Interferon Inducers interferon omega 1 Interferons Interferon Type I Lung Malignant Neoplasms Neoplasms Oncogenes Patients Pharmacotherapy Phosphorylation Proteins Psychological Inhibition Response, Immune Tumor Suppressor Genes
2
Targeting Myc Transcription Factor for Anti-Cancer Therapy
Not available on PMC !

Example 10

Myc encodes a helix-loop-helix transcription factor upregulated in 50-80% of human cancers and is associated with 100,000 US cancer deaths per year. Myc heterodimerizes with its partner Max to control target gene transcription and is deeply integrated into the regulatory and control mechanisms governing cell viability and proliferation. A recent estimate suggests that Myc binds to approximately 25,000 regions in the human genome. The loss of Myc proteins inhibits cell proliferation and growth, accelerates differentiation, increases cell adhesion, and accentuates the response to DNA damage.

We believe that Myc is an ideal target for anti-cancer therapeutics, particularly MM in which it is highly overexpressed by selective disruptive interference of Myc-Max dimerization while permiting Myc-Mad interactions.

FIG. 28 illustrates that an αvβ3 targeted particle comprising a myc prodrug reduces SMC proliferation. Human coronary smooth muscle cells were plated on cover slips (2500 cells) and incubated 2 hours. Each treatment was replicated 6 times. The intramural delivery of an αvβ3 targeted particle comprising a myc prodrug, alone or with stents, offers an attractive new approach to restenosis.

US11872313B2. Prodrug compositions, prodrug nanoparticles, and methods of use thereof (2024-01-16). Washington University [US]. Inventors: Gregory M. Lanza [US], Dipanjan Pan [US].
Patent 2024
Cardiac Arrest Cell Adhesion Cell Proliferation Cells Cell Survival Dimerization DNA Damage Genome, Human Heart Homo sapiens Malignant Neoplasms Myocytes, Smooth Muscle Obstetric Delivery Prodrugs Proteins Stents Transcription, Genetic Transcription Factor
3
Monitoring Poly(ADP-Ribosyl)ation in CHFR
Not available on PMC !

Example 3

Recruitment of PAR-dependent CHFR in U2OS cells without or with 100 nM PARG inhibitor (#34) treatment after laser scissor. We used CHRF as a readout for monitoring the level of poly(ADP-ribosyl)ation.

Laser microirradiation and imaging of cells: U2OS cells with transfection of GFP-CHFR were plated on glass-bottomed culture dishes (Mat Tek Corporation) and treated with or without 100 nM PARG inhibitor (#34). Laser microirradiation was performed using an IX 71 microscope (Olympus) coupled with the MicoPoint laser illumination and ablation system (Photonic Instruments, Inc.). A 337.1-nm laser diode (3.4 mW) transmitted through a specific dye cell and then yielded a 365-nm wavelength laser beam that was focused through 603 UPlanSApo/1.35 oil objective to yield a spot size of 0.5-1 mm. The time of cell exposure to the laser beam was ˜3.5 nsec. The pulse energy was 170 mJ at 10 Hz. Images were taken by the same microscope with the CellSens software (Olympus). GFP fluorescence at the laser line was converted into a numerical value using Image J. Normalized fluorescent curves from 50 cells from three independent experiments were averaged. The error bars represent the standard deviation.

US11858879B2. PARG inhibitors and method of use thereof (2024-01-02). City of Hope [US]. Inventors: Xiaochun Yu [US], Shih-Hsun Chen [US], Yate-Ching Yuan [US], Hongzhi Li [US], David Horne [US].
Patent 2024
blocking factor Cells DNA Damage Fluorescence Hyperostosis, Diffuse Idiopathic Skeletal Lasers, Semiconductor Light Microscopy Poly ADP Ribosylation Pulse Rate Transfection
4
Inducing DNA Damage with Ciprofloxacin
Induction of DNA-damage using ciprofloxacin was adapted from Peña et al.16 (link). Overnight cultures were subcultured in LB for 3 h at 37 °C and grown until exponential phase. The cultures were diluted to OD600 0.5 and 32 µg/ml ciprofloxacin (Sigma-Aldrich) was added to the cultures if not otherwise stated. Cultures were incubated for two hours at 37 °C and harvested by centrifuging appropriate cell numbers for the desired downstream analyses.
Eggers O., Renschler F.A., Michalek L.A., Wackler N., Walter E., Smollich F., Klein K., Sonnabend M.S., Egle V., Angelov A., Engesser C., Borisova M., Mayer C., Schütz M, & Bohn E. (2023). YgfB increases β-lactam resistance in Pseudomonas aeruginosa by counteracting AlpA-mediated ampDh3 expression. Communications Biology, 6, 254.
Publication 2023
Ciprofloxacin DNA Damage
5
Comet Assay for DNA Damage
The extent of DNA damage was evaluated based on the protocol of alkaline single-cell gel electrophoresis (comet assay) described by Tice et al. 200036 (link). Slides were examined under fluorescent microscope (Leica, Germany). For each sample, the degree of DNA migration was determined by capturing images for 50 nucleoids at 400× magnification using leica microscope camera. Analysis of comet parameters was done by using TriTek Comet Score™ Version 1.5 software. Tail length (TL), %DNA in tail and tail moment (TM) are used to evaluate the extent of DNA damage.
Ghebryal L.N., Noshy M.M., El-Ghor A.A, & Eissa S.M. (2023). Comparative analysis of Acomys cahirinus and Mus musculus responses to genotoxicity, oxidative stress, and inflammation. Scientific Reports, 13, 3989.
Publication 2023
Alkaline Comet Assay Comet Assay DNA Damage Microscopy Tail

Top products related to «DNA Damage»

1
Comet assay kit by Bio-Techne
Sourced in United States
The Comet Assay Kit is a laboratory tool used to assess DNA damage and repair at the single-cell level. It measures the extent of DNA fragmentation by evaluating the 'comet-like' tail formed during electrophoresis, which is proportional to the amount of DNA damage present in the cell.
2
Fluorescence microscope by Olympus
Sourced in Japan, United States, Germany, China, Italy, United Kingdom, Denmark, Switzerland, France
The Olympus Fluorescence Microscope is an optical microscope that uses fluorescence to visualize and analyze samples. It illuminates the specimen with light of a specific wavelength, causing fluorescent molecules within the sample to emit light at a different wavelength, which is then detected and displayed.
3
Oxiselect comet assay kit by Cell Biolabs
Sourced in United States, Germany
The OxiSelect Comet Assay Kit is a laboratory tool used to measure DNA damage in individual cells. It provides a simple and sensitive method for the detection of DNA strand breaks, alkali-labile sites, and other types of DNA damage. The kit includes all necessary reagents and components to perform the comet assay procedure.
4
Etoposide by Merck Group
Sourced in United States, Germany, United Kingdom, Japan, France, China, Italy, Canada, Switzerland, Belgium, Macao, Portugal, Poland
Etoposide is a chemotherapeutic agent used in the treatment of various types of cancer. It is a topoisomerase inhibitor that disrupts the process of DNA replication, leading to cell death. Etoposide is available as a solution for intravenous administration.
5
Fetal bovine serum (fbs) by Thermo Fisher Scientific
Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal
Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
6
4 6 diamidino 2 phenylindole (dapi) by Merck Group
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DAPI is a fluorescent dye that binds strongly to adenine-thymine (A-T) rich regions in DNA. It is commonly used as a nuclear counterstain in fluorescence microscopy to visualize and locate cell nuclei.
7
Lipofectamine 2000 by Thermo Fisher Scientific
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.
8
Hcs dna damage kit by Thermo Fisher Scientific
Sourced in United States
The HCS DNA Damage Kit is a lab equipment product designed to detect and quantify DNA damage in cells. It provides a standardized and automated approach to measure multiple DNA damage parameters simultaneously using high-content screening (HCS) technology.
9
Doxorubicin by Merck Group
Sourced in United States, Germany, United Kingdom, France, China, India, Italy, Poland, Macao, Japan, Sao Tome and Principe, Canada, Spain, Brazil, Australia, Belgium, Switzerland, Singapore, Israel
Doxorubicin is a cytotoxic medication that is commonly used in the treatment of various types of cancer. It functions as an anthracycline antibiotic, which works by interfering with the DNA replication process in cancer cells, leading to their destruction. Doxorubicin is widely used in the management of different malignancies, including leukemia, lymphoma, and solid tumors.
10
In situ cell death detection kit by Roche
Sourced in Germany, United States, Switzerland, China, United Kingdom, France, Canada, Belgium, Japan, Italy, Spain, Hungary, Australia
The In Situ Cell Death Detection Kit is a laboratory product designed for the detection of programmed cell death, or apoptosis, in cell samples. The kit utilizes a terminal deoxynucleotidyl transferase (TdT) to label DNA strand breaks, allowing for the visualization and quantification of cell death. The core function of this product is to provide researchers with a tool to study and analyze cell death processes.

More about "DNA Damage"

DNA damage is a critical cellular event that can lead to genetic instability and various diseases.
This can be caused by a variety of endogenous and exogenous factors, such as reactive oxygen species, ultraviolet radiation, and chemical agents.
Accurate detection and quantification of DNA damage is essential for understanding its underlying mechanisms and developing effective interventions.
One common method for assessing DNA damage is the Comet Assay, which uses a fluorescence microscope to measure DNA fragmentation in individual cells.
The OxiSelect Comet Assay Kit is a popular tool for this analysis.
Additionally, dyes like DAPI can be used to stain DNA and visualize cellular damage.
Drugs like Etoposide and Doxorubicin are known to induce DNA damage, and can be useful for studying the cellular response.
FBS (Fetal Bovine Serum) is often used as a cell culture supplement, while Lipofectamine 2000 is a transfection reagent that may be employed in DNA damage research.
The HCS (High Content Screening) DNA Damage Kit provides a high-throughput method for quantifying various DNA damage markers, such as γH2AX, which indicate the presence of double-strand breaks.
By utilizing AI-driven protocol optimization tools like PubCompare.ai, researchers can streamline their DNA damage studies, ensuring reproducibility and accuracy in their results.
This helps advance our understanding of this critical cellular process and the development of effective interventions.