Ontology highlight
ABSTRACT:
PROVIDER: PRJNA626661 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11575956_1.fastq.gz | Fastqsanger.gz | |||
| SRR11575956_2.fastq.gz | Fastqsanger.gz | |||
| SRR11575957_1.fastq.gz | Fastqsanger.gz | |||
| SRR11575957_2.fastq.gz | Fastqsanger.gz | |||
| SRR11575958_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:In our study we have identified MS023, an inhibitor of PRMTs, to increase SMN protein and FL SMN2 transcript levels, and to improve survival and weights of treated SMA mice, alone and in combination with currently approved antisense oligonucleotide. In order to understand the molecular underpinnings of the added benefit provided by the combinatorial treatment, we performed bulk transcriptomic analysis in spinal cords of SMA mice treated with MS023 only, nusinersen only, and MS023 in combination with nusinersen, compared to wild type and SMA littermates.
2023-03-01 | GSE206400 | GEO
Project description:scRNAseq of MS023-treated muscle stem cells.
2023-01-05 | GSE199420 | GEO
Project description:To investigate the effect of pharmacological inhibition of the type I PRMTs in ccRCC cell lines. We treated one patient derived cell line (RCC243) and one commercially available line (786-0) in duplicate with 5uM MS023 for 3 days vs. 0.1% DMSO alone. We then performed gene expression profiling analysis using data obtained from RNA-seq. Each cell line was treated as a biological replicate. Similarly, to investigate the genetic knockdown of PRMT1 using the same cell lines, stably transduced dox-inducible PRMT1 targeting shRNA's. Cell lines were treated with or with out 1ug/mL dox for 4 days in triplicate. Gene expression profiling analysis was then performed using data obtained from RNA-seq.
2024-08-16 | GSE229357 | GEO
Project description:Here, we investigate the role of enhancers in myofibroblasts, a cell type that dominates the pathogenesis and progression of tissue fibrosis. We reveal that bromodomain and extra-terminal family members (BETs), an important group of epigenetic readers, are critical for super-enhancer-mediated pro-fibrotic gene expression in hepatic stellate cells (HSCs, lipid-containing liver-specific pericytes), upon activation during liver fibrogenesis give rise to myofibroblasts2-4. We observe significantly enriched localization of BETs to hundreds of super-enhancers associated with genes involved in multiple pro-fibrotic pathways. This unique loading pattern consequentially serves as a molecular mechanism by which BETs modulate pro-fibrotic gene expression in myofibroblasts. Strikingly, suppression of BET-enhancer interaction using small-molecule inhibitors such as JQ1 dramatically blocks activation of HSCs into myofibroblasts and significantly compromises the proliferation of activated HSCs. Identification of BRD2, BRD3, BRD4, PolII, PolIIs2p and PolIIs5p binding sites in human stellate LX2 cells that were treated with DMSO (0.1%) or JQ1 (500nM) for 16 hrs.
2015-12-11 | E-GEOD-58680 | biostudies-arrayexpress
Project description:Multiple myeloma (MM) is a devastating plasma cell malignancy characterized by the expansion of aberrant monoclonal plasma cells in the bone marrow, leading to severe clinical manifestations and poor prognosis, particularly in relapsed/refractory cases. Identifying novel therapeutic targets is crucial to improve treatment outcomes in these patients. In this study, we investigated the role of protein arginine methyltransferase 1 (PRMT1) in MM pathogenesis and explored its potential as a therapeutic target. We observed that PRMT1, responsible for majority of asymmetric di-methylation in cells, exhibited the highest expression among PRMT family members in MM cell lines and primary MM cells. Importantly, PRMT1 expression was significantly elevated in relapsed/refractory patients compared to newly diagnosed patients. High expression of PRMT1 expression was strongly associated with poor prognosis. We found that genetic or enzymatic inhibition of PRMT1 impaired MM cell growth, induced cell cycle arrest, and triggered cell death. Treatment with MS023, a potent PRMT type I inhibitor, demonstrated a robust inhibitory effect on viability of primary cells isolated from both newly diagnosed and proteasome inhibitor-relapsed/refractory patients in a dose-dependent manner. In vivo studies using a xenograft model revealed that targeting PRMT1 by either CRISPR/Cas9-mediated knockout or MS023 treatment significantly attenuated MM tumor growth and prolonged the survival of tumor-bearing mice. Histological analysis further confirmed increased apoptotic cell death in MS023-treated tumors. Collectively, our findings establish PRMT1 as an indispensable and novel therapeutic vulnerability in MM. The elevated expression of PRMT1 in relapsed/refractory patients underscores its potential as a target for overcoming treatment resistance. Moreover, our results highlight the efficacy of MS023 as a promising therapeutic agent against MM, offering new avenues for therapeutic approaches in relapsed/refractory MM.
2023-06-16 | GSE234807 | GEO
Project description:Background: Differentiation of fibroblasts into myofibroblasts is necessary for wound healing, but excessive myofibroblast presence and persistence can result in scarring. Treatment for scarring is limited largely due to a lack of comprehensive understanding of how fibroblasts and myofibroblasts differ at the transcript level. The purpose of the study was to comprehensively characterize transcriptional profiles of injured fibroblasts relative to normal fibroblasts, utilizing fibroblasts from the vocal fold as a model for other areas of the body. Results: we identified differentially expressed genes between groups of normal fibroblasts, scarred fibroblasts, and fibroblasts treated with transforming growth factor-beta 1 (TGF-β1), which represented an induced-scar phenotype. Principal component analysis revealed clustering of normal fibroblasts separate from the clustering of fibroblasts treated with TGF-β1; scarred fibroblasts were more similar to normal fibroblasts than fibroblasts treated with TGF-β1. Enrichment analyses revealed pathways related to cell signaling, receptor-ligand activity, and regulation of cell functions in scarred fibroblasts, pathways related to cell adhesion in normal fibroblasts, and pathways related to ECM binding in fibroblasts treated with TGF-β1. Although transcriptomic profiles between scarred fibroblasts and fibroblasts treated with TGF-β1 were relatively dissimilar, the most highly co-expressed genes were enriched in pathways related to actin cytoskeleton binding. Conclusions: Transcriptomics of normal fibroblasts differ from myofibroblasts, including from those retrieved from scar and those treated with TGF-β1. Despite large differences in transcriptomics between tVFF and sVFF, tVFF serve as a useful in vitro model of myofibroblasts and highlight key similarities to myofibroblasts extracted from scar pathology, as well as expected differences related to normal fibroblasts from healthy VF.
2025-03-25 | GSE278852 | GEO