Testicular gene expression changes with loss of Topaz1
TOPAZ1, a germ cell specific factor, is essential for male meiotic progression.
Specimen part
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Unlinking an lncRNA from Its Associated cis Element.
Specimen part, Cell line
View SamplesTranscriptome analysis of effect of Lockd knockout on cells
Unlinking an lncRNA from Its Associated cis Element.
Specimen part
View SamplesMicroRNAs inhibit gene expression by recruiting the RNA-induced silencing complex (RISC) to mRNAs in a process termed RNA interference (RNAi). While it is generally accepted that RNAi modulates gene expression pervasively, the number of mRNAs bound and repressed by miRNAs in vivo in individual cell types remains unknown, with estimates ranging from a few hundred genes to many thousands. We examined microRNA activities in primary cells by combining genetic loss of function with RNA-sequencing, quantitative proteomics and High-Throughput Sequencing of RNA isolated by Crosslinking Immunoprecipitation (HITS-CLIP), focusing on miR-144/451, the most highly expressed microRNA locus during red blood cell (RBC) formation. We show that Argonaute (Ago) protein binds over one thousand different mRNAs in a miR-144/451-dependent manner, accounting for one third of all Ago-bound mRNAs. However, only about 100 mRNAs are stabilized in RBC precursors after ablation of the miR-144/451 locus. Thus, Ago-miRNA complexes destabilize only a small subset of bound mRNAs, probably no more than a few hundred in erythroblasts under physiological conditions. Our integrated approach identified more than 50 new miR-144/451 target mRNAs, including Cox10, which facilitates assembly of the mitochondrial cytochrome c oxidase (COX) electron transport complex. Loss of miR-144/451 resulted in increased Cox10 expression, accumulation of the COX complex, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting Cox10. Overall design: HITS-CLIP analysis of 3 WT mice fetal livers vs 3 miR-144/451 KO mice fetal livers
Regulation of gene expression by miR-144/451 during mouse erythropoiesis.
Cell line, Subject
View SamplesWe found that MPLA reprograms macrophages in a way that supports a persistent monocyte/macrophage chemokine secretion profile reflected in macrophage mRNA. Additionally, this RNA-seq data revealed that certain genes (e.g. phagocytosis-related) persist much longer after MPLA than others (e.g. pro-inflammatory cytokines). Overall design: Bone marrow derived macrophages were harvested for RNA after 4hrs of monophosphoryl lipid A (MPLA) priming, 24hrs of MPLA priming, and 3 days following the end of priming
The TLR4 Agonist Monophosphoryl Lipid A Drives Broad Resistance to Infection via Dynamic Reprogramming of Macrophage Metabolism.
Cell line, Subject
View SamplesChronic injury in kidney transplants remains a major cause of graft loss. The aim of this study was to identify a predictive gene set capable of classifying renal grafts at risk for progressive injury due to fibrosis.The Genomics of Chronic Allograft Rejection (GoCAR) study is a prospective, multicenter study. Biopsies obtained prospectively 3 months after transplantation from renal allograft recipients (n=159) with stable renal function were analyzed for gene expression by microarray. Genes were sought which correlated with subsequent 12-month Chronic Allograft Damage Index (CADI) but neither CADI in the 3 month biopsy nor other histological or clinical parameters.
Biopsy transcriptome expression profiling to identify kidney transplants at risk of chronic injury: a multicentre, prospective study.
Specimen part
View SamplesThere are a few markers for embryonic hepatic stellate cells in mouse embryonic livers
Isolation of a unique hepatic stellate cell population expressing integrin α8 from embryonic mouse livers.
Specimen part
View SamplesGlioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. Further investigation showed dbcAMP reversed Warburg effect evidenced by increase of oxygen consumption and reduction of lactate production. Stimulated mitochondrial biogenesis downstream of CREB/PGC1a pathway triggered metabolic shift and differentiation. Blocking mitochondrial biogenesis by mdivi1 or silencing PGC1a abrogated differentiation, reversely over-expression of PGC1a elicited differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induced tumor growth inhibition and differentiation. This study shows mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation process of tumor cells. Overall design: mRNA profiles of cell line DBTRG-05MG after 0h, 6h, 12h, 24h and 48h of dbcAMP treatment
The Anti-Warburg Effect Elicited by the cAMP-PGC1α Pathway Drives Differentiation of Glioblastoma Cells into Astrocytes.
Specimen part, Cell line, Subject
View SamplesThere are a few markers available to distinguish hepatic stellate cells (HSCs), portal fibroblasts (PFs), and mesothelial cells (MCs) in the adult mouse liver.
Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers.
Specimen part
View SamplesBACKGROUND: Despite the moderate incidence of papillary renal cell carcinoma
A molecular classification of papillary renal cell carcinoma.
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