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SRP150616
Homo sapiens
24 Downloadable Samples
NextSeq 500
Description
Pancreatic cancer cells transduced with sh knockdown of GRP78 Overall design: Pancreatic cancer mRNA profiles of scrambled control versus shGRP78 cell line, in triplicate, using Illumina Truseq Stranded Total-RNA library
Publication Title
ER stress sensor, glucose regulatory protein 78 (GRP78) regulates redox status in pancreatic cancer thereby maintaining "stemness".
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2500
Description
Pancreatic cancer is characterized by heavy desmoplasia. Triptolide and its water-soluble pro-drug Minnelide are extremely efficient against pancreatic cancer in animal models. However, the effects of triptolide on pancreatic cancer stromal cells are largely unknown. The aim of this project is to indentify potential cellular functions that are affected by triptolide in pancreatic cancer associated fibroblasts. Overall design: Cancer associated fibroblasts were isolated from pancreatic tumor of KPC mouse model. Cells were either untreated or treated with 100nM triptolide for 6h or 24h before RNA isolation. The RNA was quality tested using a Bioanalyzer 2100 (Agilent Technologies, CA, USA). cDNA was created by reverse transcription of oligo-dT purified polyadenylated RNA and fragmented, blunt-ended, and then ligated to barcoded adaptors. Then, the library was size selected, and the selection process was validated and quantified by capillary electrophoresis and qPCR, respectively. Samples were load on the HiSeq 2500 (Illumina Inc., CA, USA) to generate around 25 million paired-end 50bp reads for each sample.
Publication Title
Inactivation of Cancer-Associated-Fibroblasts Disrupts Oncogenic Signaling in Pancreatic Cancer Cells and Promotes Its Regression.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Luminal breast cancers express estrogen (ER) and progesterone (PR) receptors, and respond to endocrine therapies. However, some ER+PR+ tumors display intrinsic or acquired resistance, possibly related to PR. Two PR isoforms, PR-A and PR-B, regulate distinct gene subsets that may differentially influence tumor fate. A high PR-A:PR-B ratio is associated with poor prognosis and tamoxifen resistance. We speculate that excessive PR-A marks tumors that will relapse early. Here we address mechanisms by which PR-A regulate transcription, focusing on SUMOylation. We use receptor mutants and synthetic promoter/reporters to show that SUMOylation deficiency or the deSUMOylase SENP1 enhance transcription by PR-A, independent of the receptors dimerization interface or DNA binding domain. De-SUMOylation exposes the agonist properties of the antiprogestin RU486. Thus, on synthetic promoters, SUMOylation functions as an independent brake on transcription by PR-A. What about PR-A SUMOylation of endogenous human breast cancer genes? To study these, we used gene expression profiling. Surprisingly, PR-A SUMOylation influences progestin target genes differentially, with some upregulated, others downregulated, and others unaffected. Hormone-independent gene regulation is also PR-A SUMOylation dependent. Several SUMOylated genes were analyzed in clinical breast cancer database. In sum, we show that SUMOylation does not simply repress PR-A. Rather, it regulates PR-A activity in a target selective manner including genes associated with poor prognosis, shortened survival, and metastasis.
Publication Title
SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 19 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The Systemic Capillary Leak Syndrome (SCLS) is an extremely rare and potentially life-treating vascular disorder of unknown etiology. SCLS is characterized by dramatic and transient episodes of hypotensive shock and edema due to plasma leakage into peripheral tissues. The disorder has garnered increased attention during the last several years because of the resemblance of its initial presentation to more common disorders such as systemic anaphylaxis, sepsis, and acute infections with the Ebola/Marburg family of filoviruses. Although approximately 70-80% of patients with SCLS have a concurrent monoclonal gammopathy of unknown significance (MGUS), any contribution of the paraprotein to acute flares is unknown. To identify circulating factors that contribute to the onset of acute SCLS crises, we performed transcriptomic profiling of paired peripheral blood mononuclear cell fractions obtained from patients during acute attacks and convalescent intervals using microarray. 61 genes were significantly up- or downregulated more than 2.5 fold in acute samples relative to baseline. One of the most upregulated genes was ADM, which encodes the vasoactive peptide adrenomedullin. The ADM surrogate pro-ADM was markedly elevated in SCLS acute sera compared to remission samples or sera from healthy controls. Monocytes and endothelial cells (ECs) from SCLS subjects expressed significantly more ADM in response to proinflammatory stimuli compared to healthy control cells. Application of ADM to ECs exerted protective effects on vascular barrier function. These results suggest a pathogenic contribution of ADM to the profound pressor-resistant hypotension that characterizes the initial stages of SCLS.
Publication Title
Adrenomedullin surges are linked to acute episodes of the systemic capillary leak syndrome (Clarkson disease).
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
We performed the whole transcriptome analysis in Zscan4 positive ES cells (Em+) and Zscan4 negative ES cells (Em-) by using FACS-sorted MC1-ZE7 ES cells. Overall design: Whole RNA-seq in Zscan4 positive and negative cells
Publication Title
Transient bursts of Zscan4 expression are accompanied by the rapid derepression of heterochromatin in mouse embryonic stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 101 Downloadable Samples
- Illumina HiSeq 2500
Description
The experiment aimed at determing the influence of mast cell deficiency on the transcriptome of skin-infiltrating leukocytes in K14HPV16 mice at 2month and 6month of age. Overall design: Skin-inflitrating leucocytes were FACS-purified from mast cell proficient (Mcpt5-Cre-) and mast cell deficient (Mcpt5-Cre+) K14HPV16 mice. Mast cells (CD117 high, FCeR1 high) were excluded from the sorting gate. In order to control for minimal mast cell contamination during sorting from K14HPV16 Mcpt5-Cre- skin, mast cell signature transcripts were identified by comparing transcriptomes of samples fromK14HPV16 Mcpt5-Cre- mice in which mast cells were flow cytometrically included vs excluded.
Publication Title
Although Abundant in Tumor Tissue, Mast Cells Have No Effect on Immunological Micro-milieu or Growth of HPV-Induced or Transplanted Tumors.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Mus musculus
- 38 Downloadable Samples
- Illumina HiSeq 2500
Description
RNA seq was used to compare the expression profile of macrophages in presence and absense of mast cells. MB49 cells were injected i.d. into Mcpt5-Cre+ R26DTA animals and cre-negative littermates. Macrophages were sorted at 20 d.p.i. Overall design: Macrophage RNA profiles of MB49 TAMs (tumor-associated macrophages), harvested at 20 d.p.i. in MC-Proficient and MC-deficient animals
Publication Title
Although Abundant in Tumor Tissue, Mast Cells Have No Effect on Immunological Micro-milieu or Growth of HPV-Induced or Transplanted Tumors.
Sample Metadata Fields
Specimen part, Subject
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
We sought to confirm the genetic influence in the development of Ventilation-Associated Lung Injury (VALI) and, in the process, identify potential candidate genes involved in the disease by integrating differential gene expression profiling on rat lungs to a traditional strain survey analysis of the parental rat strains, VALI-sensitive Brown Norway rats versus VALI-resistant Dahl Salt Sensitive rats, comparing control (under room air ventilation) versus under high tidal volume (HTV) ventilation.
Publication Title
Use of consomic rats for genomic insights into ventilator-associated lung injury.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have previously demonstrated that pre-B-cell colony enhancing factor (PBEF) ais a biomarker in sepsis and sepsis-induced acute lung injury (ALI) with genetic variants conferring ALI susceptibility118. In the current study, we explored the mechanistic participation of PBEF in ALI and ventilator-induced associated lung injury (VIALI). Initial in vitro studies and demonstrated rhPBEF aas a direct rat neutrophil chemotactic factor in vitro producing marked in vivo increases in BAL leukocytes (PMNs) in vivo following (intratracheal injection (,IT) in C57B6 mice. These latter changes were accompanied by increased BAL levels of the PMN chemoattractants (, KC and MIP2), and modest changes in lung vascular and but were not associated with significant increasesin alveolar permeability. We next explored the potential synergism between rhPBEF administration (IT) and a mechanical ventilation model of modest VILI lung injury (4 hours, 30 ml/kg tidal volume). We and observed dramatic synergistic increases in BAL PMNs, and both BAL protein and cytokine levels (IL-6, TNF-?, KC). Gene expression profiling Microarray analysis further supported a major role for PBEF in the induction of gene modules associated with ALI and VALI (NFkB pathway, leukocyte extravasation, apoptosis, toll receptor signaling). Finally, we exposed wild type and heterozygous PBEF+/- mice (targeted deletion of a single PBEF allele deletion) to a model of severe VILImechanical ventilation-induced lung injury (4 hours, 40 ml/kg tidal volume). PBEF+/- mice were significantly protected from VIALI-associated increases in BAL protein and BAL IL-6 levels and exhibited significantly reduced expression of ALI-associated gene expression modules. Together, these results indicate that PBEF is a key inflammatory mediator intimately involved in both the development and severity of ventilator-induced ALI.
Publication Title
Essential role of pre-B-cell colony enhancing factor in ventilator-induced lung injury.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have previously demonstrated that pre-B-cell colony enhancing factor (PBEF) ais a biomarker in sepsis and sepsis-induced acute lung injury (ALI) with genetic variants conferring ALI susceptibility118. In the current study, we explored the mechanistic participation of PBEF in ALI and ventilator-induced associated lung injury (VIALI). Initial in vitro studies and demonstrated rhPBEF aas a direct rat neutrophil chemotactic factor in vitro producing marked in vivo increases in BAL leukocytes (PMNs) in vivo following (intratracheal injection (,IT) in C57B6 mice. These latter changes were accompanied by increased BAL levels of the PMN chemoattractants (, KC and MIP2), and modest changes in lung vascular and but were not associated with significant increasesin alveolar permeability. We next explored the potential synergism between rhPBEF administration (IT) and a mechanical ventilation model of modest VILI lung injury (4 hours, 30 ml/kg tidal volume). We and observed dramatic synergistic increases in BAL PMNs, and both BAL protein and cytokine levels (IL-6, TNF-?, KC). Gene expression profiling Microarray analysis further supported a major role for PBEF in the induction of gene modules associated with ALI and VALI (NFkB pathway, leukocyte extravasation, apoptosis, toll receptor signaling). Finally, we exposed wild type and heterozygous PBEF+/- mice (targeted deletion of a single PBEF allele deletion) to a model of severe VILImechanical ventilation-induced lung injury (4 hours, 40 ml/kg tidal volume). PBEF+/- mice were significantly protected from VIALI-associated increases in BAL protein and BAL IL-6 levels and exhibited significantly reduced expression of ALI-associated gene expression modules. Together, these results indicate that PBEF is a key inflammatory mediator intimately involved in both the development and severity of ventilator-induced ALI.
Publication Title
Essential role of pre-B-cell colony enhancing factor in ventilator-induced lung injury.
Sample Metadata Fields
No sample metadata fields
View Samples