Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-20193
PROVIDER: PRJNA125693 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Full title: Altered levels of MOF (member of MYST family histone acetyl transferase) and decreased levels of H4K16ac correlate with a defective DNA damage response (DDR). The human MOF gene encodes a protein that specifically acetylates histone H4 at lysine 16 (H4K16ac). Here we show that altered levels of H4K16ac correlate with a defective DNA damage response (DDR) to ionizing radiation (IR). The defect however is not due to altered expression of proteins involved in DDR. Specific inhibition of H4K16ac deacetylation in MOF-depleted cells rescued IR-induced abrogation of DDR. MOF was found associated with DNA-dependent protein kinase catalytic subunit (DNAPKcs), a protein involved in non-homologous end joining (NHEJ) repair, whose ATMdependent IR-induced phosphorylation was abrogated in MOF-depleted cells. Our data indicate that MOF depletion greatly decreased the repair of DNA double-strand breaks (DSBs) by NHEJ and homologous recombination (HR). In addition, the MOF protein activity associates with chromatin upon DNA damage and colocalizes with the synaptonemal complex in male meiocytes. We propose that MOF, through H4K16ac, plays a critical role in the cellular DNA damage response. Keywords: Cell type comparison
2010-03-15 | GSE20193 | GEO
Project description:Full title: Altered levels of MOF (member of MYST family histone acetyl transferase) and decreased levels of H4K16ac correlate with a defective DNA damage response (DDR). The human MOF gene encodes a protein that specifically acetylates histone H4 at lysine 16 (H4K16ac). Here we show that altered levels of H4K16ac correlate with a defective DNA damage response (DDR) to ionizing radiation (IR). The defect however is not due to altered expression of proteins involved in DDR. Specific inhibition of H4K16ac deacetylation in MOF-depleted cells rescued IR-induced abrogation of DDR. MOF was found associated with DNA-dependent protein kinase catalytic subunit (DNAPKcs), a protein involved in non-homologous end joining (NHEJ) repair, whose ATMdependent IR-induced phosphorylation was abrogated in MOF-depleted cells. Our data indicate that MOF depletion greatly decreased the repair of DNA double-strand breaks (DSBs) by NHEJ and homologous recombination (HR). In addition, the MOF protein activity associates with chromatin upon DNA damage and colocalizes with the synaptonemal complex in male meiocytes. We propose that MOF, through H4K16ac, plays a critical role in the cellular DNA damage response. Keywords: Cell type comparison HEK293 cells were transfected with plasmids encoding hMOF for over-expression of the histone acetyl transferase that leads to elevated levels of acetylation of Lysine 16 of histone H4. siRNA mediated knock-down of hMOF was performed to deplete the H4K16ac levels. Total RNA samples for expression profiling was obtained from wild type (293 cells without any treatment), hMOF over-expressed and hMOF knock-down 293 cell lines. Each sample was analyzed in triplicates using EGPF dsRNA treated samples as control.
2010-03-23 | E-GEOD-20193 | biostudies-arrayexpress
Project description:Altered levels of MOF and decreased levels of H4K16ac correlate with a defective DNA damage response (DDR).
2025-01-24 | E-GEOD-20193 | ExpressionAtlas
Project description:Genome instability is a potential limitation to the research and therapeutic application of induced pluripotent stem cells (iPSCs). Observed genomic variations reflect the combined activities of DNA damage, cellular DNA damage response (DDR), and selection pressure in culture. To understand the contribution of DDR on the distribution of copy number variations (CNVs) in iPSCs, we mapped CNVs of iPSCs with mutations in the central DDR gene ATM onto genome organization landscapes defined by genome-wide replication timing profiles. We show that following reprogramming the early and late replicating genome is differentially affected by CNVs in ATM deficient iPSCs relative to wild type iPSCs. Specifically, the early replicating regions had increased CNV losses during retroviral reprogramming. This differential CNV distribution was not present after later passage or after episomal reprogramming. Comparison of different reprogramming methods in the setting of defective DNA damage response reveals unique vulnerability of early replicating open chromatin to retroviral vectors. 4 cell lines, all in duplicates
2016-03-29 | E-GEOD-78717 | biostudies-arrayexpress
Project description:Genome instability is a potential limitation to the research and therapeutic application of induced pluripotent stem cells (iPSCs). Observed genomic variations reflect the combined activities of DNA damage, cellular DNA damage response (DDR), and selection pressure in culture. To understand the contribution of DDR on the distribution of copy number variations (CNVs) in iPSCs, we mapped CNVs of iPSCs with mutations in the central DDR gene ATM onto genome organization landscapes defined by genome-wide replication timing profiles. We show that following reprogramming the early and late replicating genome is differentially affected by CNVs in ATM deficient iPSCs relative to wild type iPSCs. Specifically, the early replicating regions had increased CNV losses during retroviral reprogramming. This differential CNV distribution was not present after later passage or after episomal reprogramming. Comparison of different reprogramming methods in the setting of defective DNA damage response reveals unique vulnerability of early replicating open chromatin to retroviral vectors. We isolated RNA from Ataxia-telangiectasia (A-T) patient fibroblast derived iPS cells and A-T patient fibroblasts for hybridization to the Affymetrix gene expression microarrays.
2016-03-29 | E-GEOD-78716 | biostudies-arrayexpress
Project description:ChIP-Seq profiles of MSL1, MSL2, MSl3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 in Drosophila S2 cells MSL1, MSL2, MSL3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 ChIP in Drosophila S2 cells. 1-3 biological replicates per experiment. Performed in single-read and paired-end read mode.
2012-12-11 | E-GEOD-37864 | biostudies-arrayexpress
Project description:Genome instability is a potential limitation to the research and therapeutic application of induced pluripotent stem cells (iPSCs). Observed genomic variations reflect the combined activities of DNA damage, cellular DNA damage response (DDR), and selection pressure in culture. To understand the contribution of DDR on the distribution of copy number variations (CNVs) in iPSCs, we mapped CNVs of iPSCs with mutations in the central DDR gene ATM onto genome organization landscapes defined by genome-wide replication timing profiles. We show that following reprogramming the early and late replicating genome is differentially affected by CNVs in ATM deficient iPSCs relative to wild type iPSCs. Specifically, the early replicating regions had increased CNV losses during retroviral reprogramming. This differential CNV distribution was not present after later passage or after episomal reprogramming. Comparison of different reprogramming methods in the setting of defective DNA damage response reveals unique vulnerability of early replicating open chromatin to retroviral vectors. We isolated genomic DNA from Ataxia-telangiectasia (A-T) iPSC cells derived from patient fibroblasts virus and episomal vectors, coresponding fibroblasts, normal human fibroblast derived iPSCcells, for hybridization to the Affymetrix Genome-Wide Human SNP 6.0 Array.
2016-03-29 | E-GEOD-78715 | biostudies-arrayexpress
Project description:DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.
2025-06-03 | GSE278056 | GEO
Project description:DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.
2025-06-03 | GSE278055 | GEO
Project description:DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.
2025-06-03 | GSE278054 | GEO