Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1806550.fastq.gz | Fastqsanger.gz | |||
| SRR1806560.fastq.gz | Fastqsanger.gz | |||
| SRR1806570.fastq.gz | Fastqsanger.gz | |||
| SRR1806580.fastq.gz | Fastqsanger.gz | |||
| SRR1806551.fastq.gz | Fastqsanger.gz |
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Project description:The kinetics of DNA repair and RNA synthesis recovery in human cells following UV-irradiation were assessed using nascent RNA Bru-seq and quantitative long PCR. It was found that UV light inhibited transcription elongation and that recovery of RNA synthesis occurred as a wave in the 5’-3’ direction with slow recovery and TC-NER at the 3’ end of long genes. RNA synthesis resumed fully at the 3’-end of genes after a 24-hour recovery in wild-type fibroblasts, but not in cells deficient in transcription-coupled nucleotide excision repair (TC-NER) or global genomic NER (GG-NER). Different transcription recovery profiles were found for individual genes but these differences did not fully correlate to differences in DNA repair of these genes. Our study gives the first genome-wide view of how UV-induced lesions affect transcription and how the recovery of RNA synthesis of large genes are particularly delayed by the apparent lack of resumption of transcription by arrested polymerases.
2015-03-03 | GSE65985 | GEO
Project description:The kinetics of DNA repair and RNA synthesis recovery in human cells following UV-irradiation were assessed using nascent RNA Bru-seq and quantitative long PCR. It was found that UV light inhibited transcription elongation and that recovery of RNA synthesis occurred as a wave in the 5’-3’ direction with slow recovery and TC-NER at the 3’ end of long genes. RNA synthesis resumed fully at the 3’-end of genes after a 24-hour recovery in wild-type fibroblasts, but not in cells deficient in transcription-coupled nucleotide excision repair (TC-NER) or global genomic NER (GG-NER). Different transcription recovery profiles were found for individual genes but these differences did not fully correlate to differences in DNA repair of these genes. Our study gives the first genome-wide view of how UV-induced lesions affect transcription and how the recovery of RNA synthesis of large genes are particularly delayed by the apparent lack of resumption of transcription by arrested polymerases. This study is composed of three identical experiments run in three different cell lines. For each experiment, there is one control (mock irradiated cells) and four test samples (0h, 2h, 6h and 24h after UV 10J irradiation).
2015-03-03 | E-GEOD-65985 | biostudies-arrayexpress
Project description:Transcription profiling of wild type and DNA repair-deficient cells upon exposure to ultraviolet irradiation.
2009-04-01 | E-MEXP-1968 | biostudies-arrayexpress
Project description:TIAR represses c-Myc biosynthesis following ultraviolet light irradiation
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Project description:Background: The International Space Station is an orbiting laboratory for microbial research in space, where microorganisms can be exposed to multiple extremes. Dehydrated cell clusters of extremophilic bacterium Deinococcus radiodurans have survived 3-year exposure outside the International Space Station in frames of the Tanpopo mission. We investigated the robust molecular machinery of Deinococcus radiodurans involved in its recovery after long-term space travel. Methods: The space-exposed and ground control cells of Deinococcus radiodurans were recovered in a complex medium for 5 and 15 h and investigated using integrative –omics techniques combined with electron microscopy tools. Consolidative transcriptomic, proteomic, and metabolomic analyses were performed to investigate molecular kinetics of cell recovery after 3-year exposure to low Earth orbit. Results: Ultrastructure analysis showed that Deinococcus radiodurans cells remained intact after low Earth orbit exposure for 3 years. Multiscale molecular analysis revealed significant alterations in response to long-term space travel. Key adaptations included upregulated DNA repair genes,stress response regulators, and oxidative stress scavenging enzymes. Proteins associated with transmembrane processes, cell division, and stress defence were also upregulated. Metabolomic analysis showed that only a few amino acids, sugars, and specific metabolites were more abundant after low Earth orbit exposure, suggesting energy conservation for molecular repair and regulation.Primordial stress molecule spermidine is also involved in cells recovery, helping combat the stress factors after space travel. Conclusion: Comparative –omics profile of extracted mRNA, proteins and metabolites allowed us to propose a multiscale dynamic molecular response of Deinococcus radiodurans after 3 years of space exposure. The kinetic profile with 2 timepoints during post-exposure analysis enabled the identification of foreground molecular targets employed by this microorganism in recovery after a space journey. Altogether, a multi-omics approach towards space-exposed cells revealed a strong focus on repair mechanisms, stress defence, and the utilization of external resources during the initial recovery phase. These findings expand our understanding of the molecular mechanisms employed by extremophiles to survive in space, providing implications for astrobiology and future space exploration.
2025-02-27 | E-MTAB-13969 | biostudies-arrayexpress
Project description:Ultraviolet (UV)-induced DNA lesions threaten genomic stability and are associated with skin carcinogenesis. These lesions are primarily repaired by the nucleotide excision repair (NER) pathway. However, alternative repair mechanisms and regulators are emerging as critical contributors to managing UV lesions. Here, we used a click chemistry-based proteomic approach to identify DEK and NUMA1 as novel regulators of UV-induced DNA lesion repair. Depletion of DEK or NUMA1 resulted in delayed UV lesion repair and increased cellular UV sensitivity. This was accompanied by delayed recruitment of XPF to UV-damaged sites. Notably, abnormal accumulation of proliferating cell nuclear antigen (PCNA) at UV lesions was observed in DEK- or NUMA1-depleted cells. This PCNA accumulation was not entirely dependent on NER, as it also involved contributions from apurinic/apyrimidinic endonuclease 1 (APE1), a key protein in base excision repair (BER). Co-depletion experiments revealed an epistatic relationship between DEK or NUMA1 and APE1, but not with XPA, suggesting an impaired BER in DEK- or NUMA1-depleted cells, possibly due to excessive PCNA accumulation. Our findings strongly suggest that DEK and NUMA1 facilitate efficient UV lesion removal by promoting proper NER activity and regulating APE1-mediated long-patch BER, highlighting the collaborative roles of NER and BER in UV lesion repair.
2025-12-01 | PXD061212 | Pride
Project description:Peripheral nerve injuries represent a significant clinical challenge due to their limited regenerative capacity. Surgical repair strategies include immediate nerve repair, performed shortly after injury, and delayed nerve repair, conducted after a prolonged period when primary intervention is not feasible. Understanding the molecular and genetic mechanisms underlying both strategies is essential for optimizing functional recovery. This study compares the transcriptional landscape of delayed and immediate nerve repair over time to elucidate key pathways involved in nerve regeneration. A rat model of sciatic nerve injury was used, where an 8-mm nerve gap was repaired using a chitosan conduit either immediately or after a 3-month delay. Regenerated nerves were collected at 7-, 14-, and 21-days post-repair. RNA sequencing was performed to analyze transcriptomic changes across time points, and differentially expressed genes were identified and subjected to Gene Ontology enrichment analysis to identify functional pathways and regulatory networks involved in nerve regeneration. Distinct transcriptional profiles were observed across time points after immediate and delayed repair when comparing regenerating nerves with a healthy nerve. At 7 days, both exhibited a robust inflammatory response with upregulation of genes related to cytokine signaling and myeloid cell activation. By 14 days, many pathways related to response to lipoprotein particles and phagocytosis were upregulated, with delayed repair showing downregulation of myelination-associated genes. At 21 days, immune response activation, phagocytosis and lipoprotein particle activated pathways remained upregulated in both conditions. These findings suggest that immediate repair induces a faster regenerative response, whereas delayed repair follows a slower trajectory but engages similar molecular pathways. Despite initial differences, both strategies eventually converge on key regenerative mechanisms. These insights emphasize the benefits of early intervention while highlighting the potential for delayed repair to achieve functional recovery. Future research will focus on enhancing delayed repair outcomes through targeted molecular approaches.
2025-12-23 | GSE293387 | GEO
Project description:In response to ultraviolet radiation (UVR), cells alter gene expression, switching on a variety of damage response pathways. Long non-coding RNA (lncRNA) is thought to play critical roles in regulating expression of protein-coding genes. We hypothesized that lncRNAs also regulate gene expression following UV exposure and screened for changes in lncRNA expression in human primary fibroblasts after irradiation with longwave UV (UVA) or shortwave UV (UVB).
2016-10-21 | GSE89005 | GEO
Project description:TIAR represses c-Myc biosynthesis following ultraviolet light irradiation-2
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Project description:Transcripts for GH, MHC Class I and II genes, and heavy- and light-chain myosins, as well as many others genes, were differentially regulated in the zebrafish inner ear following overexposure to sound. Following acoustic trauma in the zebrafish inner ear, we used microarray analysis to identify genes involved in inner ear repair following acoustic exposure by comparing the gene expression levels of 2 days and 4 days post-sound exposure (NE-ZF-2d and NE-ZF-4d, respectively) to controls without sound exposure (C-ZF).
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