Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA336059 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3992500.fastq.gz | Fastqsanger.gz | |||
| SRR3992501.fastq.gz | Fastqsanger.gz | |||
| SRR3992502.fastq.gz | Fastqsanger.gz | |||
| SRR3992503.fastq.gz | Fastqsanger.gz | |||
| SRR3992504.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:The long non-coding RNA Morrbid regulates Bim and short-lived myeloid cell lifespan
| PRJNA336051 | ENA
Project description:The long non-coding RNA Morrbid regulates Bim and short-lived myeloid cell lifespan (ATAC-Seq)
| PRJNA336055 | ENA
Project description:Neutrophils, eosinophils and “classical” monocytes collectively account for ~70% of human blood leukocytes and are among the shortest-lived cells in the body. Precise regulation of the lifespan of these myeloid cells is critical to maintain protective immune responses while minimizing the deleterious consequences of prolonged inflammation. However, how the lifespan of these cells is strictly controlled remains largely unknown. Here, we identify a novel long non-coding RNA (lncRNA) that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and “classical” monocytes in response to pro-survival cytokines. To control the lifespan of these cells, Morrbid regulates the transcription of its neighboring pro-apoptotic gene, Bcl2l11 (Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows for rapid control of apoptosis in response to extracellular pro-survival signals. As MORRBID is also present in humans and dysregulated in patients with hypereosinophilic syndrome, this lncRNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived myeloid cell lifespan.
2016-09-02 | GSE85072 | GEO
Project description:Neutrophils, eosinophils and “classical” monocytes collectively account for ~70% of human blood leukocytes and are among the shortest-lived cells in the body. Precise regulation of the lifespan of these myeloid cells is critical to maintain protective immune responses while minimizing the deleterious consequences of prolonged inflammation. However, how the lifespan of these cells is strictly controlled remains largely unknown. Here, we identify a novel long non-coding RNA (lncRNA) that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and “classical” monocytes in response to pro-survival cytokines. To control the lifespan of these cells, Morrbid regulates the transcription of its neighboring pro-apoptotic gene, Bcl2l11 (Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows for rapid control of apoptosis in response to extracellular pro-survival signals. As MORRBID is also present in humans and dysregulated in patients with hypereosinophilic syndrome, this lncRNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived myeloid cell lifespan.
2016-09-02 | GSE85071 | GEO
Project description:The long non-coding RNA Morrbid regulates CD8 T cells in response to viral infection
| PRJNA530996 | ENA
Project description:Deletion of several ribosomal proteins genes (RPKOs) has been shown to extend the lifespan of Saccharomyces cerevisiae in a Gcn4-dependent manner. To characterize the underlying mechanisms, we systematically analyzed the gene expression of both short- and long-lived RPKO strains at multiple levels. We found that up-regulation of amino acid biosynthesis and global down-regulation of protein synthesis are hallmarks of long-lived strains. We provide direct evidence that gene expression changes observed in long-lived strains result from translational up-regulation of GCN4 mRNA via skipping of upstream open reading frames (uORFs), in turn due to slow/defective ribosome assembly. We further demonstrate that Gcn4 acts as a transcriptional repressor on promoters of translation-related genes, thereby globally reducing protein synthesis. Our data suggest that the Gcn4-dependent increase in lifespan can be attributed partially to its ability to dampen the translation capacity of the cell, thereby engaging a well known mechanism of longevity.
2017-07-06 | PXD004760 | Pride
Project description:Mammals display wide range of variation in their lifespan. Investigating the molecular networks that distinguish long- from short-lived species has proven useful to identify determinants of longevity. Here, we compared the liver of long-lived naked mole-rats (NMRs) and the phylogenetically closely related, shorter-lived, guinea pigs using an integrated omic approach. We found that NMRs livers display a unique expression pattern of mitochondrial proteins that result in distinct metabolic features of their mitochondria. For instance, we observed a generally reduced respiration rate associated with lower protein levels of respiratory chain components, particularly complex I, and increased capacity to utilize fatty acids. Interestingly, we show that the same molecular networks are affected during aging in both NMR and humans, supporting a direct link to the extraordinary longevity of both species. Finally, we identified a novel longevity pathway and validated it experimentally in the nematode C. elegans.
2018-06-21 | PXD008720 | Pride
Project description:Identification of QTL for chronological lifespan. Pools of non-dividing, intercrossed fission yeast were sampled through time to identify alleles enriched in long-lived cells.
2018-06-25 | PRJEB27452 | EVA
Project description:Within a cell, proteins are in a dynamic state of turnover and are continuously synthesized and degraded. As an energetically expensive cellular process, protein turnover can have two opposing effects on maintaining a healthy proteome during the lifespan of an organism. Rapid protein turnover can replace old and damaged proteins with newly synthesized proteins. However, the high energetic demands of this process can potentially generate damaging reactive oxygen species that comprise the long-term health of the proteome. Thus, the relationship between aging, protein turnover kinetics and energetic demands of an organism remain unclear. Here, we used a proteomic approach to measure global rates of protein turnover within cultured fibroblasts isolated from a number of species with a wide range of lifespans. We show that organismal lifespan is negatively correlated with global rates of turnover. By further comparing cells from mice and naked mole rats (a short-lived and long-lived rodent species, respectively) we show that the latter has slower rates of turnover, lower levels of ATP production and reduced cellular ROS levels. Despite its slower rate of protein turnover, naked mole rat cells are able to tolerate protein misfolding stress more effectively than mouse cells. We suggest that in lieu of rapid constitutive protein turnover, long-lived species such as the naked mole rat have may have evolved more energetically efficient mechanisms for selective clearance of damaged proteins.
2020-05-07 | PXD018325 | Pride
Project description:Long-lived genetic mutants from different pathways of lifespan extension were used to determine the extent to which there are common downstream mediators of longevity. We have previously obtained RNA-sequencing data from other long-lived mutants including sod-2, clk-1, isp-1, nuo-6 and daf-2. Gene expression will be compared between these nine long-lived mutants.
2021-07-19 | GSE179825 | GEO