To identify genetic changes in Human Umbilical Vein Endothelial Cells induced by let-7d mimic or let-7d inhibitor transfection.
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Sex, Specimen part, Cell line, Treatment
View SamplesTo better understand the underlying molecular events, sequencing analysis was conducted by using RNAs isolated from Schwann cells treated with or without exogenous MMP7 recombinant protein.
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Sex, Specimen part, Cell line, Treatment
View SamplesTo study the global changes of genes in the dorsal root ganglion (DRG) after rat sciatic nerve injury.
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Sex, Age, Specimen part, Treatment
View SamplesThis study presented the differentially expressed genes post maize infected by Rhizoctonia solani.
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Specimen part
View SamplesTransposons in maize may be involved in the formation of circRNAs and further modulate phenotypic variation. To test our hypothesis, we performed circRNA-Seq(RNase R treated) on B73 seedlings(third leaves of V3 stage), and uncovered 1,572 high-confidence maize circRNAs, which show distinct genomic features compared to linear transcripts. Comprehensive analyses showed that LINE1-like elements (LLE) and their reverse complementary pairs (RCPLLEs) are significantly enriched in the flanking regions of circRNAs.
Circular RNAs mediated by transposons are associated with transcriptomic and phenotypic variation in maize.
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Specimen part, Disease
View SamplesWe show that key regulators of oxidative metabolism, the Estrogen Related Receptors (ERRs) and the PGC-1 co-activators, are transiently induced during somatic cell reprogramming. Bioenergetic assays reveal that while glycolysis increases throughout the reprogramming transition, the early stages feature a transient oxidative phosphorylation (OXPHOS) burst. Up-regulation of ERRa or ? is a prerequisite for the OXPHOS burst in human and mouse cells, respectively, and failure to induce this metabolic switch collapses the reprogramming process. We identify a Sca1-/CD34- sub-population of early reprogramming cells with enhanced ERR? and PGC-1ß expression as bona fide reprogramming progenitors. Transcriptional profiling confirmed that these progenitors have undergone extensive metabolic reprogramming. These studies characterize a previously unrecognized, ERR-dependent metabolic switch prior to establishment of induced pluripotency.
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No sample metadata fields
View SamplesHuman pancreatic adenocarcinoma cell line
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No sample metadata fields
View SamplesWe show that fat-resident regulatory T cells, termed fTregs, drive age-associated insulin resistance and can be specifically depleted to increase adipose insulin sensitivity. Comparative AdipoImmune profiling in young, aged, and obese mice reveals that fTregs progressively enrich in adipose as a function of age, but not obesity. fTreg-deficient mice are protected from age-associated insulin resistance and its accompanying physiological hallmarks. In contrast, fTreg-deficiency offers no protection from obesity-associated insulin resistance.
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No sample metadata fields
View SamplesTo investigate the paracrine effects of stromal elements on cancer cells, we developed a “stromal” culture system, which incorporates structural and diffusible stroma-derived elements into homotypic cultures amenable to functional genomics and metabolomics. Here we show that microenvironmental cues co-regulate cancer metabolism and gene expression. Stromal inputs broadly influenced histone acetylation in the cancer epigenome, which coincided with induction of genes implicated in anabolic metabolism and inflammation. The gene expression and metabolic changes induced by stromal factors overlap with those previously identified following oncogenic Kras, suggesting functional complementarity between cell-autonomous and microenvironmental pathways. Finally, we implicate the BET family of epigenetic readers as key transducers of stromal inputs to drive alterations in gene expression. This work suggests paracrine epigenome regulation as a conduit through which stromal signals drive metabolic and immune adaptation to a challenging tumor microenvironment.
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No sample metadata fields
View SamplesWe report that Rev-erba is targeted for ubiquitination and subsequent degradation by the F-box protein Fbxw7a, and identify the cyclin-dependent kinase 1 (Cdk1)-mediated phosphorylation of threonine 275 as necessary for the recruitment of the Fbxw7-dependent E3 ligase complex. In vitro, inhibition of Cdk1 kinase activity or mutation of T275 is sufficient to disrupt the Fbxw7-mediated Rev-erba degradation pathway. Moreover, genetic disruption of Fbxw7 in mouse liver dramatically alters the circadian expression of core clock genes and perturbs whole body lipid and glucose levels. These results reveal an additional level of regulation required for maintaining circadian rhythmicity, and reveal the essential roles of post-translational modifications in the coordination of the circadian clocks and metabolism through regulation of nuclear receptor protein stability.
No associated publication
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No sample metadata fields
View Samples