Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4116022_1.fastq.gz | Fastqsanger.gz | |||
| SRR4116022_2.fastq.gz | Fastqsanger.gz | |||
| SRR4116023_1.fastq.gz | Fastqsanger.gz | |||
| SRR4116023_2.fastq.gz | Fastqsanger.gz | |||
| SRR4116024_1.fastq.gz | Fastqsanger.gz |
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Project description:In order to study the mechanism of co-inactivation of RB1 and TP53 in the transformation of lung adenocarcinoma to small cell lung cancer, we established the NCI-H1975 cell line with RB1 knockdown.NCI-H1975 cells were cultured and infected with lentivirus expressing RB1-shRNA (n=3) or pLKO.1-shRNA (n=3), We then performed transcriptome sequencing (RNA-seq) on the above cells.
2023-08-20 | PXD042073 | Pride
Project description:The first GSSM of V. vinifera was reconstructed (MODEL2408120001). Tissue-specific models for stem, leaf, and berry of the Cabernet Sauvignon cultivar were generated from the original model, through the integration of RNA-Seq data. These models have been merged into diel multi-tissue models to study the interactions between tissues at light and dark phases.
2024-09-02 | MODEL2408160001 | BioModels
Project description:In order to investigate the potential role of TP53 in regulating translation, HCT116 wild type and TP53 knockout cells were analyzed using both RNA sequencing, Ribosome sequencing and nascent proteome analysis. The cells were treated with 0.2 µg/ml Neocarcinostatin (NCS) to induce DNA damage and activate TP53.
2022-04-27 | PXD029512 | Pride
Project description:SARS-CoV-2 induces widespread transcriptomic changes in host cells upon infection, in part through activation and modulation of innate immunity pathways and downstream gene regulation. However, the mechanisms by which SARS-CoV-2 and its evolutionary variants differentially affect host cell transcriptomic states remain largely unclear. Through chromatin proteomic (iDAPT-MS) analysis, we found that although SARS-CoV-2 and other pathogenic coronaviruses exhibit similar proteomic shifts on chromatin, SARS-CoV-2 uniquely promotes TP53 nuclear accumulation and activation. Parallel assessment of SARS-CoV-2 viral protein expression on host chromatin states (ATAC-seq) identifies intracellular spike protein as a key determinant of virus-mediated chromatin accessibility changes. Multilevel chromatin profiling reveals increased TP53 nuclear accumulation, TP53-associated chromatin accessibility changes, and TP53 target gene activation upon expression of SARS-CoV-2 alpha (B.1.1.7) and delta (B.1.617.2) spike variants relative to the ancestral spike sequence. TP53, ACE2, and furin cleavage are required for these changes, driving decreased cellular proliferation, increased cellular senescence, and increased cytokine release. Finally, BA.1 but not BA.2, BA.2.12.1, nor BA.4/BA.5 spike expression leads to attenuated TP53 activity and fusogenicity relative to ancestral spike. Our findings implicate spike-mediated host TP53 activation as a “rheostat” of COVID-19 pathogenicity.
2023-09-09 | PXD034648 | Pride
Project description:The incidence of TP53 loss-of-function in hepatocellular carcinoma is very high. In order to clarify the gene expression differences induced by the changes of TP53 gene, we used two human hepatocellular carcinoma cell lines, SK-HEP-1 and Hep 3B with TP53 knockdown or overexpression for RNA sequencing . SK-HEP-1 is a TP53 wild-type hepatocellular carcinoma cell line. Thus, we knockdown TP53 in SK-HEP-1. Hep 3B is a TP53 loss-of-function hepatocellular carcinoma cell line. Thus, we overexpress TP53 in Hep 3B. Results of RNA-seq analysis showed the differences after knocking-down or overexpressing TP53.
2023-12-06 | GSE240197 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare TP53-WT and TP53-KO HCT116 cells transcriptome profiling (RNA-seq) under 5-FU treatment condition and to evaluate the correlation between transcriptome profileing and chromatin accessibility under 5-FU treatment. Methods: HCT116 cell profiles of TP53-WT and TP53- KO were generated by deep sequencing, in duplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform levels: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA). Conclusions: Our study represents the detailed analysis of TP53-WT and TP53-KO HCT116 cell transcriptomes under 5-FU treatment with different timepoint, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that RNA-seq offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a TP53-WT and TP53-KO cells with and without 5-FU treatment in different timepoint. We conclude that NGS based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2021-02-10 | GSE157951 | GEO
Project description:Zebrafish SHH MB tumors were generated by CRISPR-Cas9-mediated mutation of ptch1 in the context of tp53 heterozygous and tp53 mutant animals. Gene expression of the entire brain for ptch1 crispant animals and tp53 mutant control animals was analyzed by RNA-seq.
2024-07-09 | GSE242897 | GEO
Project description:A single copy loss of CTCF is found in about 50% of breast cancer patients. Based on clinical TCGA data we hypothesized that the loss of CTCF may potentiate TP53 target gene expression in patients. Using MCF10A cells as a model, we deleted a single copy of CTCF using CRISPR/Cas9. We found, using qPCR and RNA-seq, that cells carrying low CTCF displayed an enhanced TP53 response after exposure to chemotherapeutics. Using ATAC-seq, we aimed to explore whether the elevated induction of TP53 target gene transcription was associated with changes in open or closed chromatin structure. Specifically, we were interested in comparing chromatin accessibility at TP53 target genes within MCF10A CTCF +/- cells compared to control cells following the induction of DNA damage (6uM cisplatin for 8h). We discovered that accessibility of the transcription start site is associated with heightened gene expression in CTCF+/- compared to the control. Interestingly, for a subset of TP53 response genes, there is increased accessibility on both transcriptional start sites and termination sites following the induction of DNA damage. The importance of chromatin accessibility at these two regions is still under investigation. Additionally, accessible gene regions at both sites also appear to have greater enrichment within TADS in the CTCF+/- cell compared to the control. We propose that the increased accessibility of TP53 target genes following damage represents a mechanism enhancing the efficacy of the TP53-regulated DNA damage response.
2023-11-10 | GSE217698 | GEO
Project description:Background: Although TP53 gain-of-function (GOF) mutations promote cancer survival, its effect on EGFR-TKI efficacy remains unclear. We established EGFR-mutant lung cancer cell lines expressing various TP53 genotypes using CRISPR-Cas9 technology and found that TP53-GOF mutant cells develop an early resistance to EGFR-TKI osimertinib.The goal of this study is to elucidate the mechanisms underlying resistance to osimertinib treatment in TP53 GOF mutations through comprehensive gene analysis using ChIP-seq.
2024-01-22 | GSE253478 | GEO