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916 results for “DNA damage”
Data from: A significant component of ageing (DNA damage) is reflected in fading breeding colors: an experimental test using innate antioxidant mimetics in painted dragon lizards
A decade ahead of their time, von Schantz and coworkers united sexual selection and free radical biology by identifying causal links between deep-rooted physiological processes that dictate resistance to toxic waste from oxidative metabolism (reactive oxygen species), and phenotypic traits, such as ornaments. Ten years later, these ideas have still only been tested with indirect estimates of free radical levels (oxidative stress) subsequent to the action of innate and dietary antioxidants. Here we measure net superoxide (a selection pressure for antioxidant production) and experimentally manipulate superoxide antioxidation using a synthetic mimetic of superoxide dismutase, Eukarion 134 (EUK). We then measure the toxic effect of superoxide in terms of DNA erosion and concomitant loss of male breeding coloration in the lizard, Ctenophorus pictus. Control males suffered more DNA damage than EUK-males. Spectroradiometry showed that male coloration is lost in relation to superoxide and covaries with DNA erosion; in control males these variables explained 72 % of color loss, whereas in EUK males, the fading of coloration was unaffected by superoxide and unrelated to DNA damage. Thus, EUK's powerful antioxidation removes the erosion effect of superoxide on coloration and experimentally verifies the prediction that colors reflect innate capacity for antioxidation.
Figure 5 in Comparative analysis of the karyotype sensitivities of Apodemus flavicollis and laboratory mice to DNA-damaging agents
Figure 5. Polyploid metaphase in bone marrow cell of A. flavicollis after Mitomycin C treatment. Some of the chromosomes are also damaged. Pericentric inversions and fragments are observed.
ATM-ESCO2-SMC3 axis promotes 53BP1 recruitment in response to DNA damage and safeguards genome integrity by stabilizing cohesin complex
<p>53BP1 is primarily known as a key regulator in DNA double-strand break (DSB) repair. However, the mechanism of DSB-triggered cohesin modification-modulated chromatin structure on the recruitment of 53BP1 remains largely elusive. Here we identified acetyltransferase ESCO2 as a regulator for DSB-induced cohesin-dependent chromatin structure dynamics, which promotes 53BP1 recruitment. Mechanistically, in response to DNA damage, ATM phosphorylates ESCO2 S196 and T233. MDC1 recognizes phosphorylated ESCO2 and recruits ESCO2 to DSB sites. ESCO2-mediated acetylation of SMC3 stabilizes cohesin complex conformation and regulates the chromatin structure at DSB breaks, which is essential for the recruitment of 53BP1 and the formation of 53BP1 microdomains. Furthermore, depletion of ESCO2 in both colorectal cancer cells and xenografted nude mice sensitizes cancer cells to chemotherapeutic drugs. Collectively, our results reveal a molecular mechanism for the ATM-ESCO2-SMC3 axis in DSB repair and genome integrity maintenance with a vital role in chemotherapy response in colorectal cancer.</p>
ATM-ESCO2-SMC3 axis promotes 53BP1 recruitment in response to DNA damage and safeguards genome integrity by stabilizing cohesin complex
<p>53BP1 is primarily known as a key regulator in DNA double-strand break (DSB) repair. However, the mechanism of DSB-triggered cohesin modification-modulated chromatin structure on the recruitment of 53BP1 remains largely elusive. Here we identified acetyltransferase ESCO2 as a regulator for DSB-induced cohesin-dependent chromatin structure dynamics, which promotes 53BP1 recruitment. Mechanistically, in response to DNA damage, ATM phosphorylates ESCO2 S196 and T233. MDC1 recognizes phosphorylated ESCO2 and recruits ESCO2 to DSB sites. ESCO2-mediated acetylation of SMC3 stabilizes cohesin complex conformation and regulates the chromatin structure at DSB breaks, which is essential for the recruitment of 53BP1 and the formation of 53BP1 microdomains. Furthermore, depletion of ESCO2 in both colorectal cancer cells and xenografted nude mice sensitizes cancer cells to chemotherapeutic drugs. Collectively, our results reveal a molecular mechanism for the ATM-ESCO2-SMC3 axis in DSB repair and genome integrity maintenance with a vital role in chemotherapy response in colorectal cancer.</p>
Fig. 5 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 5. Nerolidol suppressed the protein and mRNA expression of ATM in rat leiomyoma cells. (A, B) ELT3 cells were treated with nerolidol for 48 h and were then harvested for the western blot analysis of phosphorylated ATM and total ATM (A) and for determining ATM mRNA expression using quantitative RT-PCR (B). GAPDH was used as the loading control. The inserted numbers in (A) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (C, D, E, F) ELT3 cells were treated with the indicated concentrations of KU-55933, an ATM inhibitor, for 48 h, following which the cells were harvested for further analysis. (C) The expression levels of p-ATMser1981, total ATM, p-Aktser473, total Akt, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (D, E) Cell cycle analysis was performed after propidium iodide staining and FACS, and the results were analyzed using the FlowJo software (D). The percentages of cells in each cell cycle phase are plotted in (E). (F) Cell proliferation was determined using the MTT assay. DMSO (0.1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the control group.
Fig. 3 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 3. Nerolidol treatment led to the generation of intracellular ROS and impaired the mitochondrial membrane potential. (A) ELT3 cells were harvested after trypsin/EDTA treatment and then treated with 20 mM NAC, followed by DCFDA staining for 30 min. The cells were then treated with nerolidol for another additional 30 min, and DCF fluorescence was detected using flow cytometry. H2O2 was used as the positive control. The data were analyzed using the FlowJo software. (B, C) ELT3 cells were harvested and treated with nerolidol for 30 min. The cells were then stained with JC-1 dye for 15 min, followed by flow cytometry analysis. FCCP was used as the positive control. The data were analyzed using the FlowJo software. (B) The gated cells in the graphs indicate the cells with low mitochondrial membrane potential, and the quantitative results are plotted in (C). (D) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 5 mM NAC. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. (E) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 20 μM ferrostatin-1. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-values were calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; ***, p <0.001 compared to the vehicle control group (C). ***, p <0.001 compared to the nerolidol single treatment group (D, E).
Fig. 4 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 4. Treatment with nerolidol triggered DNA damage in rat leiomyoma cells. (A, B) ELT3 cells were harvested and treated with 100 μM nerolidol for 30 min, followed by determination of DNA damage using the comet assay. H2O2 (200 μM) was used as the positive control. The tail moments are indicated by red arrows in (A), as quantified using a live video imaging system, and dot plots show the mean ± SD in (B). (C, D, E) ELT3 cells were treated with 100 μM nerolidol for 1 h, followed by incubation with anti-p-γH2AXser139 antibody and FITC-conjugated secondary antibody. Nuclei were visualized using DAPI (blue). (C) P-γH2AXser139 expression was quantified using an automated imaging system. The relative positive cell number and the nuclear p-γH2AXser139 intensities are plotted in (D) and (E), respectively. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2. Nerolidol induced G1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 2. Nerolidol induced G1 cell cycle arrest by downregulating Akt phosphorylation and cell cycle-related proteins. ELT3 cells were treated with the indicated concentrations of nerolidol for 48 h and were then harvested after trypsin/EDTA treatment. (A, B) For cell cycle analysis, the harvested cells were fixed with 70 % ethanol, followed by propidium iodide staining, and the DNA content was measured using flow cytometry. The results were analyzed using the FlowJo software (A). Blue, olive green, and green represent the G1, S, and G2/M phases, respectively. The percentage of each cell cycle phase was plotted in (B). The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group.*, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (C) Total cellular protein content was measured, and the expression levels of phosphorylated Akt, total Akt, cyclin D1, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) indicate the relative expression level compared to that of the vehicle control (indicated as 0 μM). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 1. Nerolidol inhibited the proliferation of rat leiomyoma cells. ELT3 cells were seeded in 24-well plates and treated with the indicated concentrations of nerolidol for 48 h. (A) Images were captured under an inverted microscope at 100 × magnification. (B) The cells were trypsinized, and the number of viable (upper panel) or dead (lower panel) cells was counted after staining with trypan blue with a hemocytometer. (C) Cell proliferation was also determined using the MTT assay. Ethanol (1 %) was used as the vehicle control, which is indicated as 0 μM. The data are presented as relative percentage compared to the vehicle control. The p-value was calculated using one way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05 and ***, p <0.001 compared to the vehicle control group. The IC50 values were calculated using the IC50 Calculator (https://www.aatbio.com/tools/ic50-calculator).
Study of the Effect of SNPs in p53 and p53 Response Elements on the Inflammatory Response to DNA Damage
ClinicalTrials.gov study NCT01143519. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Analysis of Androgene Receptors Axis and DNA Damage Repair Genes in Patients With Prostate Cancer
ClinicalTrials.gov study NCT03677414. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Changes in Anthropometric, Biochemical and DNA Damage Parameters After 3-weeks VLCD in Severely Obese Patients
ClinicalTrials.gov study NCT05007171. IPD Sharing: NO. Countries: 1. Publications: 18.
Effect of Modified Fujita Technique Uvulopalatoplasty on Oxidative DNA Damage Levels in Patients With Obstructive Sleep Apnea SyndromE (OSAS)
ClinicalTrials.gov study NCT01635699. IPD Sharing: Not stated. Countries: 1. Publications: 1.
DNA Damage & Repair Proteins In Patients With Atherosclerotic Coronary Artery Disease
ClinicalTrials.gov study NCT02335086. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Cutaneous DNA Damage Caused by UV-A Irradiation
ClinicalTrials.gov study NCT00864955. IPD Sharing: Not stated. Countries: 1. Publications: 5.
A Phase II Study of Nivolumab in Patients With Genetic Alterations in DNA Damage Repair and Response Who Progressed After Standard Treatment for Metastatic Solid Cancers
ClinicalTrials.gov study NCT04761744. IPD Sharing: NO. Countries: 1. Publications: 33.
Melatonin and DNA Damage Study
ClinicalTrials.gov study NCT03945955. IPD Sharing: NO. Countries: 1. Publications: 3.
The Role of DNA Damage of Granulosa Cell on Oocyte Quality and in Vitro Fertilization Outcome
ClinicalTrials.gov study NCT03345030. IPD Sharing: NO. Countries: 1. Publications: 3.
In-depth comparative toxicogenomics of glyphosate and Roundup herbicides: Histopathology, transcriptome and epigenome signatures, and DNA damage
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Data from: Interspecific hybrids show a reduced adaptive potential under DNA damaging conditions
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