Similar Datasets
Project description:Burkholderia pseudomallei OS strain:OS Genome sequencing and assembly
| PRJNA188496 | ENA
Project description:The osdcl4-1 mutant exhibits much severer developmental defects than dcl4 in Arabidopsis, suggesting that Os DCL4 may process broader substrates in rice. By deep sequencing of small RNAs from different tissues of wild types and osdcl4-1, we revealed that 21-nucleotide siRNAs were largely dependent on Os DCL4. Besides several tasiRNA loci reported in Arabidopsis and rice, over one thousand 21-nucleotide and several dozen 24-nucleotide phased siRNA (phasiRNA) clusters were identified in panicles but not in seedlings and grains. Further analyses identified two conserved 22-nucleotide motifs among the cleavage sites of the 21- and 24- phasiRNA loci, and the cleavage sites of over 90% of 21- and 24-nucleotide phasing clusters were confirmed by PARE/degradome analysis from 93-11 panicles. MiR2118 and miR2275, expressed specifically in panicles, were predicted to trigger cleavages at 21- and 24-nucleotide phasiRNA clusters, respectively. The triggers of phasiRNAs are more dependent on Os DCL4 than Os DCL1. Furthermore, the processing of 21-nucleotide phasiRNAs was largely Os DCL4-dependent, whereas the processing of 24-nucleotide phasiRNAs was slightly affected by Os DCL4, but not by Os DCL3a and Os DCL1. Our results revealed distinct roles of Os DCL4 in a novel 21- and 24-nucleotide phasiRNA biogenesis pathway in rice.
2012-03-30 | GSE22763 | GEO
Project description:Genome sequence of Comamonadaceae bacterium strain OS-1and OS-4
| PRJDB14719 | ENA
Project description:To explore possible oncogenic factors in OS, we used a microarray-based approach to profile changes in the expression of miRNAs in five OS cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profile in the miRNA expression of OS
2015-07-01 | GSE70367 | GEO
Project description:Vitiligo is a skin disease characterized by the destruction of epidermal melanocytes due to oxidative stress and autoimmune response. As the main responder to oxidative stress, keratinocytes facilitate melanocyte loss under oxidative stress by inducing melanocyte death and recruiting antigen-specific CD8+ T cell to skin to destroy melanocytes. It has been proved that keratinocytes secrete abundant functional exosomes, but the role of exosomes secreted from keratinocytes under oxidative stress in vitiligo pathogenesis is unknown. We found that oxidative stress enhanced the secretion of exosomes from keratinocytes. These exosomes (OS-Exos) administration aggravated melanocyte loss and CD8+ T cell infiltration in the epidermis of tail in the vitiligo mouse model, thereby driving vitiligo progression. OS-Exos suppressed the survival of melanocytes while promoting the proliferation and activation of CD8+ T cells in vitro. As miRNAs contained in OS-Exos might be responsible for the functions of OS-Exos on melanocytes and CD8+ T cells, we employed small RNAs-seq analysis to screen miRNAs enriched in OS-Exos as compared to those in Exos (from untreated HaCaT cells). The hierarchical clustering analysis and the volcano plot showed the distinct signatures of known miRNAs as well as novel miRNAs between OS-Exos and Exos. In total, 276 differentially expressed miRNAs were discovered, with 134 and 142 miRNAs displaying significant up- or down-regulation, respectively, in OS-Exos compared with Exos (P<0.05; fold change≥2. The above data suggest that miRNAs enriched in OS-Exos might contribute to the facilitatory role of OS-Exos in vitiligo progression.
2023-10-23 | GSE245757 | GEO
Project description:Effective therapies for metastatic osteosarcoma (OS) remain a major clinical unmet need. Targeting mRNA translation in metastatic OS represents an attractive option, as selective translation under stress supports the rapid synthesis of cytoprotective proteins that facilitate metastatic competence. We therefore assessed eukaryotic translation factors in OS, revealing high expression of eIF4A1 in metastatic OS. The eIF4A1 inhibitor, CR-1-31B, potently inhibited metastatic OS growth in vitro and reduced lung tumor burden in orthotopic mouse models. CR-1-31B synergized with the oxidative stress inducer, tert-butylhydroquinone (tBHQ), to enhance cell death under oxidative stress. Proteomic analysis revealed a subset of proteins that were upregulated by tBHQ alone, but inhibited by co-treatment of CR-1-31B, most notably the NRF2 antioxidant transcription factor, and NRF2 inactivation phenocopied CR-1-31B in blocking OS lung metastasis in vivo. Collectively, our data reveal that targeting eIF4A1 with CR-1-31B is highly effective in blocking OS metastasis by blunting the NRF2 antioxidant response.
2024-07-16 | PXD047420 | Pride
Project description:Osteosarcoma (OS)is a rare primary malignant bone tumor in adolescents and children with a poor prognosis. Identification of prognostic genes lags far behind the advance of the treatments. We identified differential genes by microarray analysis from paired OS tissues. Hub genes, gene set enrichment analysis, and pathway analysis were performed to gain an insight into the pathway alterations of OS. These results showed CPE could be served as a prognostic factor in osteoblastic OS and should be further investigated as potential therapeutic target. The present study evaluated the whole transcriptome expression of osteosarcoma progression and provided novel therapeutic targets for advanced osteosarcoma.
2023-03-01 | GSE225588 | GEO
Project description:To investigate whether IDO1 participated in OS malignant progression through miRNA, we selected non-metastatic OS cell line (MG63), metastatic OS cell line (143B) and non-tumorigenic immortalized osteoblastic hFOB1.19 cell line as the research object. Over Expression cell lines are contructed and exosomal miRNAs from both control and OE cell lines are sequenced to find out the differences in expression in the exosomes secreted from IDO1 overexpressing and WT cells.
2023-05-14 | GSE232452 | GEO