Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2338217_1.fastq.gz | Fastqsanger.gz | |||
| ERR2338217_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Rhodococcus sp. CX strain:CX Genome sequencing and assembly
| PRJNA678864 | ENA
Project description:We discovered two small molecule drugs - CX-5461 and CX-3543 - with specific toxicity against BRCA deficiencies in cancer cells and xenograft models. Both CX-5461 and CX-3543 have been previously recognized as RNA pol I inhibitors. CX-5461 is in advanced phase 1 trials for treatment of lymphoma and leukemia through rDNA transcription inhibition in a p53-dependent mechanism. We have discovered a novel activity of CX-5461, as a stabilizer of G-quadruplex DNA sequences inside cells the same as CX-3543. We found that BRCA1 and BRCA2 deficiency markedly increases (one log order) sensitivity to CX-5461 and a related drug CX-3543 in human cancer cell lines and polyclonal patient derived xenograft models, providing a direct therapeutic hypothesis, including PDX tumours resistant to PARP inhibition. We show that in epithelial cells, exposure to CX-5461 and CX-3543 blocks replication forks and induces ssDNA gaps or breaks. The BRCA and NHEJ pathways are required for the repair of CX-5461 and CX-3543 induced DNA damage and failure to do so leads to lethality. RNA pol I inhibition is not a required component of the cell killing mechanism in these tumours, because BRCA2 deficient cells are not more sensitive to BMH-21, a more potent rDNA transcription inhibitor. These data strengthen the concept of G4 targeting as a therapeutic approach, specifically for targeting HR and NHEJ deficient cancers and other tumors deficient for DNA damage repair. Since CX-5461 is already in advanced phase 1 trials for other indications, this has resulted in immediately testable translational implications (Canadian trial, NCT02719977, opened May 2016) as no phase-1 eligible G4 stabilizers have been described to date.
2016-12-06 | GSE90967 | GEO
Project description:Yimella sp. cx-51 isolate:cx-51 Genome sequencing
| PRJNA715956 | ENA
Project description:Microbacterium sp. cx-55 isolate:cx-55 Genome sequencing
| PRJNA784401 | ENA
Project description:Kocuria sp. cx-51 isolate:cx-51 Genome sequencing
| PRJNA715954 | ENA
Project description:Culex pipiens pallens and Cx. p. quinquefasciatus are important vectors of many diseases, such as West Nile fever and lymphatic filariasis. The widespread use of insecticides to control these disease vectors and other insect pests has led to insecticide resistance becoming common in these species. High throughput screening using SSH and specific microarray platforms was thought to have identified some resistance-related genes. However, limitations of these methods meant that only a few hundred of the many thousand genes could be screened. It wasn’t until the sequencing of the Cx. quinquefasciatus genome in 2010 that it became possible to screen all 18.9 thousand genes in the mosquito genome for anti-insecticidal activity. We used high throughout Illumina sequencing to identify hundreds of Cx. p. pallens and Cx. p. quinquefasciatus genes that were differentially expressed in response to pesticide exposure. The identification of these genes is a vital first step for more detailed investigation of the molecular mechanisms involved in insecticide resistance in mosquitoes. In this study, larvae of Cx. pipiens pallens and Cx. pipiens quinquefasciatus were collected from field and transported to the laboratory and reared to adulthood to get F1 generation. Then, half of the F1 generation was conducted to pesticide bioassay. RNA extraction and Illumina sequencing were undertaken in another half of the F1 generation. Therefore, Samples used in Illumina sequencing did not contact any insecticides. Twelve Cx. pipiens pallens and Cx. pipiens quinquefasciatus lavae were undertaken Illumina RNA sequencing.
2014-05-07 | E-GEOD-57307 | biostudies-arrayexpress
Project description:Sequencing files from TRAP-seq samples isolated from DHPG-stimulated WT and Fmr1-/y hippocampal slices incubated with vehicle or 200 nM CX-5461
2022-06-07 | GSE200919 | GEO
Project description:We demonstrate that CX-5461 treatment suppresses multiple canonical pathways and transcriptions factors We used microarrays to analyze the potential mechanism by which CX-5461 regulates gene expression.
2022-12-21 | GSE201899 | GEO
Project description:CX-5461 (CX) is a clinical-stage anticancer agent originally identified as an RNA polymerase I inhibitor, but more recently recognized for its ability to target the beta isoform of topoisomerase II (TOP2B). This isoform is also inhibited by anthracyclines such as Doxorubicin (DOX), a widely used chemotherapy drug known to cause cardiotoxicity. To investigate whether CX shares similar cardiotoxic potential, we compared its effects to DOX in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from six donors. Both drugs induced cell death, yet CX was markedly less cytotoxic than DOX, with an approximate 20-fold difference in potency. At sub-lethal concentrations, DOX led to significant DNA damage, whereas CX did not. Transcriptome analysis was performed across three timepoints following treatment with low and high sub-micromolar doses of each drug. Gene expression profiling revealed that DOX triggered extensive transcriptional reprogramming involving thousands of genes, while CX elicited a more restrained response affecting only hundreds. Time-course comparisons showed partial overlap in gene response trajectories, with CX-responsive genes representing a subset of the broader DOX-induced network. These shared genes were enriched for pathways involved in chromosome segregation and DNA replication. Importantly, analysis of genes located within functionally validated loci implicated in anthracycline-induced cardiotoxicity demonstrated that DOX altered the expression of ~80% of these genes, whereas CX had no measurable effect. These findings suggest that although CX can engage certain transcriptional programs similar to DOX, its overall impact on cardiomyocytes is substantially attenuated and does not resemble the cardiotoxic signature characteristic of DOX exposure.
2025-12-11 | GSE302122 | GEO