Irradiation induced bone marrow ablation ultimately enhanced PTH anabolic effects in bone.
An irradiation-altered bone marrow microenvironment impacts anabolic actions of PTH.
Specimen part, Treatment
View SamplesRNA-Seq was used to profile transcriptional changes induced by overexpression of the long non-coding RNA SLNCR1, as well as mutant version SLNCR1 delta conserved and SLNCR1 conserved. Overall design: The A375 melanoma cell line was transfected with pcDNA3.1 (-) expressing either full length SLNCR1, SLNCR1 delta conserved, or SLNCR1 conserved.
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
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View SamplesRNA-Seq was used to profile transcriptional changes induced by siRNA knockdown of the long non-coding RNA SLNCR1. Overall design: The WM1976 melanoma short-term culture was transfected with either scrambled or SLNCR1-targeting siRNAs
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
No sample metadata fields
View SamplesWe sequenced mRNA from zebrafish wild-type embryos, gata5 morphants, gata6 morphants, and gata5/6 morphants at bud and 6-somite developmental stages to identify genes co-operatively regulated by gata5 and gata6 during cardiomyocyte progenitor specification. Overall design: Samples were collected in duplicate, with 40 embryos per sample. Single 36-base pair reads were sequenced on the Illumina Genome Analyzer IIx
Tmem88a mediates GATA-dependent specification of cardiomyocyte progenitors by restricting WNT signaling.
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View SamplesPurpose: identify genes regulated by expression of miR-31 in primary mouse CD8 T-cells by exogenously expressing pre-miR-31 from the Plko.3g lentiviral vector. Cells infected with empty Plko.3g vectors were used as controls for infection.
The microRNA miR-31 inhibits CD8<sup>+</sup> T cell function in chronic viral infection.
Specimen part
View Samples-cell identity is determined by tightly regulated transcriptional networks that are modulated by extracellular cues, thereby ensuring -cell adaptation to the organisms insulin demands. We have observed in pancreatic islets that stimulatory glucose concentrations induced a gene profile that was similar to that of freshly isolated islets, indicating that glucose-elicited cues are involved in maintaining -cell identity. Low glucose induces the expression of ubiquitous genes involved in stress responses, nutrient sensing, and organelle biogenesis. By contrast, stimulatory glucose concentrations activate genes with a more restricted expression pattern (- and neuronal- cell identity). Consistently, glucose-induced genes are globally reduced in islets deficient with Hnf1a (MODY3), characterized by a deficient glucose metabolism. Of interest, a cell cycle gene module was the most enriched among the variable genes between intermediate and stimulatory glucose concentrations. Glucose regulation of the islet transcriptome was unexpectedly broadly maintained in islets from aged mice. However, the cell cycle gene module is selectively lost in old islets and the glucose activation of this module is not recovered even in the absence of the cell cycle inhibitor p16.
Glucose regulation of a cell cycle gene module is selectively lost in mouse pancreatic islets during ageing.
Specimen part
View SamplesArabidopsis thaliana ecotype Columbia glabra were grown for 4 days in the dark without added sucrose. Samples were subsequently kept for 6h either [1] under aerobic conditions, [2] under anoxia in absence of sucrose or [3] under anoxia in presence of sucrose.
A genome-wide analysis of the effects of sucrose on gene expression in Arabidopsis seedlings under anoxia.
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View SamplesWe used microarrays to compare the global programme of gene expression in primary cultures of neurons and astrocytes. These data sets were compared to the expression profiles of other tissues, including pancreatic islets, in order to identify a specific neuroendocrine program in pancreatic islets.
Glucose regulation of a cell cycle gene module is selectively lost in mouse pancreatic islets during ageing.
Specimen part
View SamplesMurine pancreatic beta cell line MIN6 was growth at two different concentrations of glucose (22,2 and 5,5 mM of glucose), 37C, 5% CO2 and was treated at four different concentrations of human amylin (0, 1, 10 and 20 uM) during three different times (2, 12 and 24 hours)
Impairment of the ubiquitin-proteasome pathway is a downstream endoplasmic reticulum stress response induced by extracellular human islet amyloid polypeptide and contributes to pancreatic beta-cell apoptosis.
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View SamplesPTBP1 and PTBP2 control alternative splicing programs during neuronal development, but the cellular functions of most PTBP1/2-regulated isoforms remain unknown. We show that PTBP1 guides developmental gene expression by regulating the transcription factor Pbx1. We identify exons that are differentially spliced when mouse embryonic stem cells (ESCs) differentiate into neuronal progenitor cells (NPCs) and neurons, and transition from PTBP1 to PTBP2 expression. We define those exons controlled by PTBP1 in ESCs and NPCs by RNA-seq analysis after PTBP1 depletion and PTBP1 crosslinking-immunoprecipitation. We find that PTBP1 represses Pbx1 exon 7 and the expression of its neuronal isoform Pbx1a in ESC. Using CRISPR-Cas9 to delete regulatory elements for exon 7, we induce Pbx1a expression in ESCs, finding that this activates transcription of specific neuronal genes including known Pbx1 targets. Thus PTBP1 controls the activity of Pbx1 and suppresses its neuronal transcriptional program prior to differentiation. Overall design: 46C mESCs were differentiated in mNPCs. The mNPCs were treated with 10 nM control, Ptbp1, Ptbp2, or Ptbp1 and Ptbp2 siRNAs for 48 hours. The knockdowns were performed using 2 independent sets of siRNAs. Poly-A RNA was isolated for RNA-sequencing and splicing analyses.
The splicing regulator PTBP1 controls the activity of the transcription factor Pbx1 during neuronal differentiation.
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View Samples