Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA274699 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:UV (UVC, 10J/m2) light irradiation effect on human hepatoma Hep3B cells
| PRJNA274700 | ENA
Project description:UV (UVC, 10J/m2) light irradiation effect on Ewing Sarcoma cells
| PRJNA256994 | ENA
Project description:UV-induced CPDs were mapped in isolated human genomic DNA following 80J/m2 of UVC irradiation
2021-08-27 | GSE162125 | GEO
Project description:UV-induced 6-4PPs were mapped in normal human skin fibroblasts following 500J/m2 of UVC irradiation
2021-08-27 | GSE175590 | GEO
Project description:human hepatoma Hep3B cells were treated with 40 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-02-06 | GSE65676 | GEO
Project description:human hepatoma Hep3B cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-10-20 | GSE65678 | GEO
Project description:human hepatoma Hep3B cells were treated with 40 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression. Three biological replicates were labeled in direct and dye-swap microarray experiments and hybridized onto an Agilent custom splicing-sensitive microarray platform
2015-02-06 | E-GEOD-65676 | biostudies-arrayexpress
Project description:To further study and understand the DNA damage responses, we developed aniFOUND, a new method for capturing under native conditions the repaired DNA and the proteins associated with it after UVC irradiation. hTert-immortalised human skin fibroblasts were irradiated with 20 J/m2 UVC and the nascent DNA that resulted from the Unscheduled DNA Synthesis was specifically labeled with nucleotide analogues (EdU). This newly repaired/synthesized DNA together with the bound proteins were pulled-down with streptavidin beads. For negative controls we used both irradiated, but non-labelled samples (+UV/-EdU) and labelled, but not irradiated cells (-UV/+EdU). The pulldowns were eluted from the beads by boiling in 0.1 % SDS.
2021-03-10 | PXD012997 | Pride
Project description:To monitor the changes in transcription and alternative splicing upon UV irradiation, human hepatoma Hep3B cells were Hep3B cells were washed two times with PBS and then irradiated with 40J/m2 UV light; fresh medium was immediately added after the irradiation and the cells were incubated at 37 C and collected 6 hours after the treatment for the RNA preparation. RNAs from three biological replicates of control or irradiated cells were purified, reverse transcribed into cDNA, labelled with Cy5 or Cy3 fluorochromes, and hybridized to a custom splicing-sensitive microarray<br>cDNA and Cy5-Cy3 labelled cRNA were generated from the total RNA using the Agilent Low RNA Input Fluorescent Linear Amplification kit; the cRNA was purified with the RNeasy Mini kit (Qiagen). 8?g of each cRNA were used for the hybridization with the arrays (Agilent In situ hybridization kit plus). After hybridization, arrays were washed, and scanned images analyzed. Three biological replicates were hybridized, with both direct and dye-reversal hybridizations. General gene expression values represent the average of log2 ratios for all the probes in constitutive exones of a locus. Statystical analyses were carried out with Linear Models for Microarray Data (Limma; Bioconductor Project; Dudoit, et al., 2003). The background correction method used in the analysis was Normexp (Ritchie, et al., 2007). Locally weighted linear regression (LOWESS) analysis was used as a normalization method (Yang, et al., 2002).<br>
2009-07-10 | E-MEXP-2353 | biostudies-arrayexpress
Project description:Transcriptional profiling of HepG2 cells treated with UVC (254 nm) for 30 seconds and transduced with Adenoviral vector carrying the Hepatitis B Virus HBx gene vs Adenoviral vector control under UV treatment Experiment Overall Design: One-condition experiment, AdHBx (experimental) UV vs AdEasy (vector control) UV. HepG2 cells were infected with either recombinant HBx adenoviruses (AdHBx) or control adenoviruses (AdEasy). Seventy-two hours later, infected cells were exposed for 30 seconds to UVC (254 nm) irradiation with a germicidal lamp calibrated to deliver 8 or 16 J/m2. Cells were then harvested for either ChIP-chip profiling or expression microarray profiling
2008-10-21 | E-GEOD-11064 | biostudies-arrayexpress