Bulk RNA-seq from Trex1 KO in heart
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Mus musculus
SUBMITTER: Katherine Williams
PROVIDER: E-MTAB-16524 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The DNA exonuclease TREX1 degrades endogenous cytosolic DNA. Cytosolic DNA triggers the cGAS/STING pathway which increases type I interferon. To investigate the physiological significance of TREX1 loss on in vivo tumor growth, we implanted control and TREX1-deficient CT26 tumor cells into immunocompetent BALB/c hosts.Tumor cells were collected 7 days after tumors reached around 200mm3.
2024-03-12 | E-MTAB-13816 | biostudies-arrayexpress
Project description:We performed bulk RNA-seq on cell lines with and without knock out of the Trex1 gene.
2024-03-12 | E-MTAB-13815 | biostudies-arrayexpress
Project description:Single-cell RNA-seq data for Trex1 WT and KO mice from the heart. Used for manuscript in submission at Science Advances.
2026-03-25 | E-MTAB-16525 | biostudies-arrayexpress
Project description:Single-cell RNA-seq data for Trex1 WT and KO mice from the tumor. Used for manuscript in submission at Science Advances.
2026-03-25 | E-MTAB-16526 | biostudies-arrayexpress
Project description:Double-stranded RNA (dsRNA) is an established trigger of innate immunity, activating intrinsic and extrinsic cellular response mechanisms. While this response is typically associated with viral infection, it has also been shown that accumulation of self-derived dsRNAs known as endoge-nous dsRNA, also have the capacity to activate similar innate pathways. However, the extent to which endogenous dsRNA is dynamically regulated during normal cellular non-immune homeo-stasis, as opposed to pathological states, remains poorly understood. This raises important ques-tions about the physiological roles of dsRNA and the mechanisms that restrain its immunostimu-latory potential. Here, we aim to characterize the presence of endogenous dsRNA within the skin at steady state and understand its accumulation during differentiation, wound healing and within hair follicle stem cell niches. We find that dsRNA is predominantly localized to basal progenitor epidermal keratinocytes under homeostatic conditions and is upregulated in wound healing areas that later harbor neogenic hair follicle morphogenesis. Notably, we also observed upregulation of dsRNA during a transient state of hair follicle stem cell activation, suggesting a role in maintain-ing progenitor multipotency and directing early differentiation. Given the essential role of dsRNA and its capacity to induce regeneration, uncovering the mechanisms that govern its accumulation will reveal the regulatory machinery that influences cell fate and holds therapeutic potential.
2026-02-12 | PXD073594 | Pride
Project description:The ATP binding cassette (ABC) transporter family is widely distributed in vertebrates and is essential for drug resistance, cell signaling and energy homeostasis. There is growing evidence that various ABC transporters contribute to the growth and development of tumors but relatively little is known about how the ABC transporter family behaves in hepatocellular carcinoma (HCC). ABCC6 transporter was downregulated in HCC tissues and that it was associated with successful treatment for HCC patients. Cellular model studies have shown that ABCC6 plays a role in the migration and cytoskeleton rearrangement of HepG2 hepatocarcinoma cells, highlighting its role in cancer biology. Abcc6-silenced HepG2 cells are used as cell model to obtain more deep information about the molecular mechanisms underlying the observed results. MTT and colony formation assays, showed the effects of Abcc6 on HepG2 cell proliferation. Western blotting analysis, real-time PCR, and immunofluorescence were used to find the E-cadherin, Vimentin, and N-cadherin markers associated with the epithelial-to-mesenchymal transition (EMT). Colony formation experiments in the current study showed that Abcc6 decreased HepG2 cell viability. The migratory and invasion activities were dramatically slowed down by Abcc6 silencing, according to the Transwell and wound-healing assays. In tumor cells, EMT has been shown to be crucial for enhancing migration and invasion and is frequently characterized by a loss of epithelial markers (E-cadherin) and an increase in mesenchymal markers (Vimentin and N-cadherin). In the western blotting examination, E-cadherin expression was considerably elevated compared to the control group, while N-cadherin and Vimentin expression were downregulated. This led to the hypothesis that the underlying mechanism of Abcc6 knockdown prevents migration and invasion in HepG2 cells and is linked to the suppression of EMT. In conclusion all evidence suggested that ABC transporters play a more active role in cancer biology.
2024-01-02 | E-MTAB-13154 | biostudies-arrayexpress
Project description:To better understand the mechanism underlying the invasion and migration phenotype instigated by EFEMP1 EVs (extracellular vesicles), we performed RNA sequencing analysis on BT549 cells treated with control and EFEMP1KD EVs.
2025-09-13 | E-MTAB-14473 | biostudies-arrayexpress
Project description:Profiling open chromatin in different tissue types around the gastro-oesophageal junction to allow for clustering of samples and investigation of transcription factor binding site motif enrichment.
2021-08-24 | E-MTAB-10044 | biostudies-arrayexpress
Project description:Triple negative breast cancer (TNBC) is a highly heterogeneous disease representing the most aggressive breast cancer (BC) subtype. Lack of Estrogen Receptor alpha (ERα), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/neu) expression makes TNBC immune to common therapies, significantly limiting the treatment options and suggesting the need to identify novel therapeutic targets. It was previously reported that Estrogen Receptor beta (ERβ) is expressed in a fraction of TNBC patients, where its presence correlates with improved patient outcome. Recently, we demonstrated an oncosuppressive ERβ effect in TNBC cell models expressing exogenous ERβ. On the other hand, it was shown that ERβ is involved in miRNA-mediated gene regulation in hormone-responsive BC cells, suggesting similar effect also in TNBC. To verify this hypothesis, we performed small non-coding RNA (sncRNA) sequencing on three engineered cell lines belonging to different TNBC molecular subtypes. ERβ-specific changes of sncRNA profile revealed that the major part of deregulated molecules are subtype specific, with only few commonly regulated ones. In order to validate the obtained results, we performed sncRNA profiling of 12 ERβ positive and 32 ERβ negative TNBC tissues, whose receptor status was assessed by immunohistochemistry in our previous research. Also here, ERβ-specific group of deregulated sncRNAs was identified. Interestingly, comparison of obtained in vitro and in vivo results revealed 2 differentially expressed miRNAs, displaying the same behavior in all three analyzed cell lines and tissues. In concordance with our previous results, IPA signaling pathway analysis performed on genes targeted by deregulated miRNAs highlighted downregulation of cholesterol biosynthesis pathway and upregulation of several signaling processes. Taken together, these findings suggest that ERβ is able to exert its oncosuppressive role in TNBC through miRNA-mediated regulation of gene expression.
2020-04-04 | E-MTAB-8807 | biostudies-arrayexpress
Project description:Huntington's disease (HD) is a late-onset, progressive, neurodegenerative disorder, usually in the second decade of life, with a fatal outcome in about 6 to 20 years after onset. Many studies have focused on the dysregulation of noncoding RNAs (ncRNAs), such as microRNAs (miRNAs), which play a regulatory function on messenger RNAs (mRNAs) by degrading or inhibiting them. Since abnormal gene expression underlies many diseases, miRNAs are thought to exert influence on several aspects. Differential expression analysis was conducted on patient vs. control samples using the Bioconductor DESeq2 package. Instead, to perform miRNA-target analysis, clusterProfiler was used to study functional target analysis. Specifically, clusterProfiler analysis was based on Gene Ontology (GO - Cellular Component (CC), Biological Process (BP) and Molecular Function (MF)) and KEGG pathway database, selecting a set of miRNAs with padj≤0.05 and |fold-change|≥1.5. Differential expression analysis between the two groups revealed 270 miRNAs were significantly upregulated (fold change ≥ 1.5), while 519 were significantly downregulated (fold change ≤ -1.5). The enrichment analysis allowed us to identify a large number of functional terms associated with the target genes of dysregulated miRNAs. In particular, among the terms we focused on: positive regulation of cell development and nucleocytoplasmic transport, vacuolar membrane and chromosome, centromeric region and, finally DNA-binding transcription factor binding and nuclear receptor binding.
2025-10-10 | E-MTAB-15153 | biostudies-arrayexpress