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SRP030399
Arabidopsis thaliana
10 Downloadable Samples
Illumina HiSeq 2000
Description
To understand how atypical bHLH, INCREASED LEAF INCLINATION1 (ILI1)-BINDING bHLH-1 (IBH1) (At2g43060), and close homologue, IBH1-like1 (IBL1) (At4g30410), interact to regulate cell elongation, genome-wide RNA-Seq expression analyses of IBH1 and IBL1 gain-(IBH1OE, IBL1OE) and loss-of-function (ibh1 (SALK 049177), ibl1(SALK 119457)) mutants were conducted. Overall design: For loss-of-function mutant, homozygous ibh1(SALK 049177) and ibl1(SALK 119457) were compared to wild type (Col). For gain-of-function mutant, homozygous 35Spro:IBH1-GFP and 35Spro:IBL1-GFP were compared to wild type (Col). Total RNAs were extactced from seedling of each genotypes. For each genotype two biological replicates were sequenced.
Publication Title
Helix-loop-helix/basic helix-loop-helix transcription factor network represses cell elongation in Arabidopsis through an apparent incoherent feed-forward loop.
Sample Metadata Fields
Specimen part, Subject
View Samples- Sus scrofa
- 39 Downloadable Samples
Affymetrix Porcine Genome Array (porcine)
Description
Experiments on primary cultures of native and regenerated endothelial cells demonstrated genomic changes in the latter related to vasomotor control, coagulation, oxidative stress, lipid metabolism and extracellular matrix. However, the genomic changes caused by the combination of either hyperlipidemia or supplementation with polyunsaturated fatty acids and endothelial regeneration are unknown.The present experiments were designed to test the hypothesis that endothelial regeneration process is affected differentially at the genomic level by the exposure to either high cholesterol or PUFA-rich diet in vivo.
Publication Title
Differential genomic changes caused by cholesterol- and PUFA-rich diets in regenerated porcine coronary endothelial cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
C57Bl6J mice were injected CCL4 for 8 weeks to induce liver injury and livers were used to prepare RNA.
Publication Title
Interspecies NASH disease activity whole-genome profiling identifies a fibrogenic role of PPARα-regulated dermatopontin.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
Skin conventional dendritic cells (cDC) exist as two distinct subsets, cDC1 and cDC2, which maintain the balance of immunity to pathogens and tolerance to self and microbiota. Here we examined the roles of dermal cDC1 and cDC2 during bacterial infection, notably Propionibacterium acnes (P. acnes). cDC1, but not cDC2, regulated the magnitude of the immune response to P. acnes in the murine dermis by controlling neutrophil recruitment to the inflamed site and survival and function therein. Single-cell mRNA sequencing revealed that this regulation relied on secretion of the cytokine VEGFa by a minor subset of activated EpCAM+CD59+Ly6D+ cDC1. Neutrophil recruitment by dermal cDC1 was also observed during S. aureus, BCG or E. coli infection, as well as in a model of bacterial insult in human skin. Thus, skin cDC1 are essential regulators of the innate response in cutaneous immunity, with roles beyond classical antigen presentation. Overall design: Examined the effect of cDC1 (CD103+DC) depletion on neutrophils infiltrating the skin during P. acnes infection.
Publication Title
A Subset of Type I Conventional Dendritic Cells Controls Cutaneous Bacterial Infections through VEGFα-Mediated Recruitment of Neutrophils.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Background: Identifying individuals at heightened cardiovascular risk is a priority for reducing the global burden of cardiovascular disease. Aspirin is widely used to prevent cardiovascular events, though with variable results. Therefore, we hypothesized that aspirin exposure would reveal novel biological pathways relevant to the development of cardiovascular events. Methods: We administered aspirin, followed by peripheral blood RNA microarray profiling, in a discovery cohort of healthy volunteers (n = 50, HV1), followed by two validation cohorts of healthy volunteers (n = 53, HV2) or outpatient cardiology (OPC, n = 25) patients, in conjunction with platelet function testing with the platelet functions score (PFS, HV1 and HV2) or the VerifyNow Asprin (VN, OPC) test. Sets of coexpressed genes, or Factors were identified via Bayesian sparse factor analysis and associated with platelet function in HV1 and validated in HV2 and OPC. Validated factors were associated with death/MI in observational (n = 191) and case:control (n = 447) patient cohorts with available RNA data collected at the time of cardiac catheterization. Results: Factor analysis yielded 20 Factors, of which one, Factor 14, contained 60 genes and was associated with PFS in HV1 (r = -0.31, p-value = 0.03). Factor 14 was associated with platelet function with the same strength and direction in HV2 (r = -0.34, p-value = 0.02) and OPC (one-sided p-value for aspirin resistant vs. aspirin sensitive = 0.046), thus validating the association. Factor 14 was associated with death/MI in the two patient cohorts, odds ratio (OR) = 1.2, 95% CI [1.02-1.4], p-value = 0.01 and hazard ratio = 1.5, [1.2-1.9], p = 0.001, respectively, independent of known cardiovascular risk factors (combined OR = 1.2, CI = [1.02, 1.4], p = 0.03). Factor 14 and the expression of the Factor 14 transcript most highly correlative of PFS, ITGA2B, improved reclassification compared to traditional risk factors (category-free net reclassification index = 31% and 37%, p 0.0002 for both). Conclusions: By challenging humans subjects with aspirin, a medication used for cardiovascular risk reduction, we elucidated genes and pathways that may underlie platelet function and mechanisms responsible for cardiovascular death/MI.
Publication Title
Aspirin insensitive thrombophilia: transcript profiling of blood identifies platelet abnormalities and HLA restriction.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2000
Description
Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34+ thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from GSI treated T-ALL cell lines, ex vivo isolated Notch active CD34+ and Notch inactive CD4+CD8+ thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publically available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T-cell context. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way towards development of novel therapeutic strategies that target hyperactive Notch1 signaling in human T-cell acute lymphoblastic leukemia. Overall design: CUTLL1 cell lines were treated with Compound E (GSI) or DMSO (solvent control). Cells were collected 12 h and 48 h after treatment. This was performed for 3 replicates. RNA-sequencing was performed on these samples.
Publication Title
The Notch driven long non-coding RNA repertoire in T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina Genome Analyzer
Description
Glucocorticoid resistance (GCR) is defined as an unresponsiveness to the anti-inflammatory properties of glucocorticoids (GCs) and their receptor, the glucocorticoid receptor (GR). It is a serious problem in the management of inflammatory diseases and occurs frequently. The strong pro-inflammatory cytokine TNF induces an acute form of GCR, not only in mice, but also in several cell lines, e.g. in the hepatoma cell line BWTG3, as evidenced by impaired Dexamethasone (Dex)-induced GR-dependent gene expression. We report that TNF has a significant and broad impact on the transcriptional performance of GR, but no impact on nuclear translocation, dimerization or DNA binding capacity of GR. Proteome-wide proximity-mapping (BioID), however, revealed that the GR interactome is strongly modulated by TNF. One GR cofactor that interacts significantly less with the receptor under GCR conditions is p300. NF?B activation and p300 knockdown both reduce transcriptional output of GR, whereas p300 overexpression and NF?B inhibition revert TNF-induced GCR, which is in support of a cofactor reshuffle model. This hypothesis is supported by FRET studies. This mechanism of GCR opens new avenues for therapeutic interventions in GCR diseases Overall design: Examination of GR induced gene expression in 4 conditions (1 control: NI and 3 treated: DEX, TNF, TNFDEX) starting from 3 biological replicates
Publication Title
TNF-α inhibits glucocorticoid receptor-induced gene expression by reshaping the GR nuclear cofactor profile.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 48 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Integrated miRNA and mRNA expression profiling in inflamed colon of patients with ulcerative colitis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In this study, we investigated if miRNA expression in UC mucosa is altered and correlated our findings with mucosal mRNA expression. Integration of mRNA and miRNA expression profiling may allow the identification of functional links between dysregulated miRNAs and their predicted target mRNA.
Publication Title
Integrated miRNA and mRNA expression profiling in inflamed colon of patients with ulcerative colitis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 19 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
T-cell/histiocyte rich B cell lymphoma (THRBL) and nodular lymphocyte predominant Hodgkin's lymphoma (NLPHL) share some morphological characteristics, including a prominent stromal reaction, but display a markedly different prognosis. To investigate the difference between the stromal reactions of these lymphomas at the molecular level, we performed microarray expression profiling on a series of THRBL and NLPHL cases.
Publication Title
T-cell/histiocyte-rich large B-cell lymphoma shows transcriptional features suggestive of a tolerogenic host immune response.
Sample Metadata Fields
Sex, Specimen part
View Samples