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GSE16983
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Parathyroid hormone (PTH) plays an essential role in regulating calcium and bone homeostasis in the adult, but whether PTH is required at all for regulating fetal-placental mineral homeostasis is uncertain. To address this we treated Pth-null mice in utero with 1 nmol PTH (1-84) or saline and examined placental calcium transfer 90 minutes later. It was found that placental calcium transfer increased in Pth-null fetuses treated with PTH as compared to Pth-null fetuses treated with saline. Subsequently, to determine the effect of PTH treatment on placental gene expression, in a separate experiment, 90 minutes after the fetal injections the placentas were removed for subsequent RNA extraction and microarray analysis.
Publication Title
Parathyroid hormone regulates fetal-placental mineral homeostasis.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Danio rerio
- 4 Downloadable Samples
IlluminaHiSeq4000
Description
We report high-throughput profiling of gene expression from whole zebrafish ventricles. We profile mRNA in uninjured ventricles and those undergoing regeneration 14 days after genetic ablation. This study provides a framework for understanding transcriptional changes during adult models of regeneration. Overall design: Examination of gene expression in cardiomyocytes under different states of proliferation.
Publication Title
Resolving Heart Regeneration by Replacement Histone Profiling.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
We used microarrays to identify transcripts regulated by dexamethasone in omental (Om) and abdominal subcutaneous (Abdsc) adipose tissues of severely obese females obtained during elective surgeries.
Publication Title
Depot Dependent Effects of Dexamethasone on Gene Expression in Human Omental and Abdominal Subcutaneous Adipose Tissues from Obese Women.
Sample Metadata Fields
Specimen part, Disease stage, Treatment
View Samples- Mus musculus
- 36 Downloadable Samples
- Illumina HiSeq 2500
Description
Purpose: The goal of this study is to analyze the transcriptional pathways regulated by Fbxo22 and Keap1 in mouse lung adeno carcinoma cells. Methods: mouse lung adeno carcinoma cells either Keap1 wild type (KP) or mutant (KPK), have been transfected for 3 days with siRNA targeting Fbxo22. Knock down efficiency has been evaluated by western blot (using specific antibody for Fbxo22) and qPCR (using specific oligos for Fbxo22) . Results: The transcriptomic analysis helps us to support our finding that loss of either Keap1 or Fbxo22 induces metastases Overall design: All 12 samples generated by deep sequencing in triplicate
Publication Title
Nrf2 Activation Promotes Lung Cancer Metastasis by Inhibiting the Degradation of Bach1.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MicroRNA-Offset RNA Alters Gene Expression and Cell Proliferation.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Drosophila melanogaster
- 9 Downloadable Samples
- Illumina HiSeq 2500
Description
Mammalian insulin and IGF induce similar but not identical changes in gene expression downstream of their respective receptors. Signaling bias at the receptor differentiates the two similar ligands, though the precise mechanism is not entirely understood. We used Drosophila insulin-like peptides DILP2 and DILP5 to determine how similar insulin-like ligands regulate similar and distinct patterns of gene expression in S2 cells by RNA-Seq. Overall, DILP2 and DILP5 stimulate many of the same changes in gene expression. However, some genes are uniquely regulated by DILP2 or by DILP5. Shared and distinct gene targets were validated by q-RT-PCR with indepedent replicates. Some unique gene targets of DILP2 are involved in sugar metabolism, which is functionally related in vivo to DILP2 and not DILP5. We find that gene expression is largely regulated in parallel by DILP2 and DILP5 but some key unique targets may lead to differential physiological functions for the two insulin-like genes. Overall design: mRNA profiles from S2 cells treated with DILP2, DILP5 or solvent were sequenced on an Illumina HiSeq2500
Publication Title
<i>Drosophila</i> Insulin-Like Peptides DILP2 and DILP5 Differentially Stimulate Cell Signaling and Glycogen Phosphorylase to Regulate Longevity.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
MicroRNA-offset RNAs (moRs) were first identified in simple chordates and subsequently in mouse and human cells by deep sequencing of short RNAs. MoRs are derived from sequences located immediately adjacent to microRNAs (miRs) in the primary miR (pri-miR). Currently moRs are considered to be simply a by-product of miR biosynthesis that lack biological activity. Here we show for the first time that a moR is biologically active. We now demonstrate that endogenous and over-expressed moR-21 significantly alters gene expression and inhibits the proliferation of vascular smooth muscle cells (VSMC). We report that the seed region of moR-21 as well as the seed match region in the target gene 3'UTR are indispensable for moR-21-mediated gene down-regulation. We further demonstrated that moR-21-mediated gene repression is Argonaute 2 (Ago2) dependent. In addition, we find that miR-21 and moR-21 may regulate different genes in a given pathway and can oppose each other in regulating certain genes. Taken together, these findings provide the first evidence that microRNA offset RNA regulates gene expression and is biologically active.
Publication Title
MicroRNA-Offset RNA Alters Gene Expression and Cell Proliferation.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- IlluminaHiSeq2000
Description
Direct conversion of somatic cells into neurons holds great promise for regenerative medicine. However, neuronal conversion is relatively inefficient in human cells compared to mouse cells. It has been unclear what might be the key barriers to reprogramming in human cells. We recently elucidated an RNA program mediated by the polypyrimidine tract binding protein PTB to convert mouse embryonic fibroblasts (MEFs) into functional neurons. In human adult fibroblasts (HAFs), however, we unexpectedly found that invoking the documented PTB–REST–miR-124 loop generates only immature neurons. We now report that the functionality requires sequential inactivation of PTB and the PTB paralog nPTB in HAFs. Inactivation of nPTB triggers another self-enforcing loop essential for neuronal maturation, which comprises nPTB, the transcription factor BRN2, and miR-9. These findings suggest that two separate gatekeepers control neuronal conversion and maturation and consecutively overcoming these gatekeepers enables deterministic reprogramming of HAFs into functional neurons. Overall design: Six RNA-seq libraries are generated by MAPS approach. Total RNA is extracted from induced neuronal cells derived from control shRNA or PTB shRNA treated human adult fibroblasts. Please note that the ''RNA-seq HAF hygro'' sample was on 6 days after switching to N3 media *without* nPTB depletion. The other two ''shPTB 6d'' and ''shPTB 3w'' were on 6 days and 3 weeks respectively after switching to N3 media *with* nPTB depletion.
Publication Title
Sequential regulatory loops as key gatekeepers for neuronal reprogramming in human cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic ß cells. Mounting evidence supports a central role for ß-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in ß cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in ß cells by inflammatory mediators play a key role in initiating the autoimmune response. We analyzed DNA methylation (DNAm) patterns and gene expression in human islets exposed to IFNa, a cytokine associated with T1D development. We found that IFNa triggers DNA demethylation and increases expression of genes controlling inflammatory and immune pathways. We then demonstrated that DNA demethylation was caused by up-regulation of the exoribonuclease, PNPase Old-35 (PNPT1), which caused degradation of miR-26a. This in turn promoted the up-regulation of ten-eleven translocation TET2 enzyme and increased 5-hydoxymethylcytosine levels in human islets and pancreatic ß-cells. Moreover, we showed that specific IFNa expression in the ß cells of IFNa-INS1CreERT2 transgenic mice, led to development of T1D that was preceded by increased islet DNA hydroxymethylation through a PNPT1/TET2-dependent mechanism. Our results suggest a new mechanism through which IFNa regulates DNAm in ß cells, leading to changes in expression of genes in inflammatory and immune pathways that can initiate islet autoimmunity in T1D. Overall design: We exposed human pancreatic islets from three donors to 2000 IU IFNa and assessed gene expression by RNAseq. The cDNA library was prepared using Illumina TruSeq RNA Sample Prep Kits. Next generation sequencing was performed on Illumina HiSeq2000 using the Single-Read Cluster Generation kit v2 and SBS Sequencing kit v3. Image analysis and base calling were conducted using the SDS 2.5/RTA1.5 software.
Publication Title
Epigenetic modulation of β cells by interferon-α via PNPT1/mir-26a/TET2 triggers autoimmune diabetes.
Sample Metadata Fields
Specimen part, Disease stage, Treatment, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours.
Publication Title
Epigenetic genome-wide analysis identifies BEX1 as a candidate tumour suppressor gene in paediatric intracranial ependymoma.
Sample Metadata Fields
Specimen part, Treatment
View Samples