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accession-icon GSE26975
Human lupus netting neutrophils induce endothelial damage, infiltrate tissues and expose immunostimulatory molecules
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our group has proposed that low-density granulocytes (LDGs) play an important role in lupus pathogenesis, as they can damage endothelial cells and synthesize increased levels of proinflammatory cytokines and type I interferons. LDGs have a heightened capacity to synthesize neutrophil extracellular traps (NETs). NETs from LDGs display increased levels of bactericidal and immunostimulatory proteins, such as the cathelicidin LL37 and externalize double-stranded DNA (dsDNA). Lupus netting LDGs have increased capacity to kill endothelial cells and expose IL-17. Through NETosis, lupus neutrophils stimulate plasmacytoid DCs to synthesize IFN-. Our results further expand the potential pathogenic role of aberrant lupus neutrophils through a NET-mediated effect.

Publication Title

Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE24110
Regression of Cardiac Hypertrophy and Attenuation of Progression to Heart Failure by Paricalcitol Therapy in Rats
  • organism-icon Rattus norvegicus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Background: Vitamin D deficiency is associated with cardiac hypertrophy and heart failure, and vitamin D therapy prevents the progression of cardiac hypertrophy in animal models. Here, we examine whether vitamin D therapy regresses pre-existing cardiac hypertrophy, and prevents the progression to heart failure.

Publication Title

Preventing progression of cardiac hypertrophy and development of heart failure by paricalcitol therapy in rats.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon SRP126064
transcriptomic profiling of HEK293 cells upon individual knockdown of the splicing factors RBM17, U2SURP or CHERP
  • organism-icon Homo sapiens
  • sample-icon 92 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We found that the core spliceosomal proteins RBM17, U2SURP and CHERP form a protein complex regulating alternative splicing and expression of a whole network of RNA binding proteins Overall design: RNA sequencing of triplicate RNA samples from HEK293 cells treated with siRNAs against RBM17, U2SURP , CHERP or SCRAMBLE sequence

Publication Title

RBM17 Interacts with U2SURP and CHERP to Regulate Expression and Splicing of RNA-Processing Proteins.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP076034
Genome-wide identification of transcription factor ATOH1 target genes in adult small intestine and colon.
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We generated three mRNA expression profiles by RNA-Seq of (i) wild-type crypts, (ii) Atoh1 knockout crypts, and (iii) purified ATOH1-positive cells. Overall design: We isolated Atoh1 knockout and littermate wild-type crypts from 6-8 week old Atoh1lox/lox;VilCreERT2 and Atoh1lox/WT;VilCreERT2 mice, respectively. In addition, ATOH1-positive cells were isolated by flow cytometry of 7AAD-negative (live), GFP-positive cells from either ileal or colonic crypts of Atoh1GFP/GFp mice (which express a functional ATOH1::GFP protein and are phenotypically normal).

Publication Title

Transcriptional Regulation by ATOH1 and its Target SPDEF in the Intestine.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP071321
Extensive cryptic splicing upon loss of RBM17 and TDP43 in neurodegeneration models
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Translating ribosome affinity purification technology was used to isolate mRNAs from cerebellar Purkinje neurons from control (Pcp2-BacTrap; Rbm17 f/+) and mutant (Pcp2-BacTRAP; Pcp2-Cre; Rbm17 f/-) mice. Overall design: RNA isolation was performed when animals were four-weeks-old (n=3 animals per genotype). Using NuGEN Ovation RNA-Seq System v2, purified double-stranded cDNA was generated from 10 ng of total RNA and amplified using both 3' poly (A) selection and random priming. 2 µg of each sample was sheared using the Covaris S2 focused-ultrasonicator following the manufacturer's protocol to obtain a final library with insert size of 400 bp. The sheared samples were quantified using the NanoDrop ND-1000 spectrophotometer and Invitrogen Qubit 2.0 DNA quantitation assay. The fragment sizes were confirmed on the Agilent Bioanalyzer to verify proper shearing. A double-stranded DNA library was produced using Illumina TruSeq DNA library preparation system and the sequencing was run on a HiSeq 2500 system.

Publication Title

Extensive cryptic splicing upon loss of RBM17 and TDP43 in neurodegeneration models.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE54054
Expression data from mouse liver
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hepatocellular carcinoma (HCC) is a deadly disease, often unnoticed till the late stages, where treatment options become limited. Thus, there is a critical need to identify early biomarkers for detection of the developing HCC, as well as molecular pathways that would be amenable to therapeutic intervention. While efforts using human serum and tissues from late stage patients have been undertaken, progress has been limited. We have therefore explored the possibility of utilizing established mouse models for the discovery of biomarkers, as well as to understand in a systematic manner the molecular pathways that are progressively deregulated by the various etiological factors in contributing to HCC formation. As an initial effort, we have used the Hepatitis B surface antigen (HBsAg) transgenic mice as a hepatitis model, which have been exposed to aflatoxin B1 (AFB1). In this report, we present the initial findings from a extensive longitudinal study, which confirms the synergistic effect of both these etiological factors, with a gender bias towards male mice. Tumors from the mouse models were validated both histologically as well as by molecular transcriptome analysis by comparison with human HCCs. In addition, using these models, we have identified carnitine as a novel biomarker for HCC development, which was again validated using human HCC samples. Conclusion: This study therefore highlights the utility of these mouse models in identifying biomarkers for detection of human HCCs, as well as for the systematic analysis of molecular pathways that are affected by various etiological agents during the progression of HCC from an untransformed hepatocyte, which could provide novel options for targeted therapy.

Publication Title

Molecular characterization of hepatocarcinogenesis using mouse models.

Sample Metadata Fields

Specimen part

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accession-icon GSE88721
miRNA and gene expression data from meningioma samples and healthy meningial cell line
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Simultaneous analysis of miRNA-mRNA in human meningiomas by integrating transcriptome: A relationship between PTX3 and miR-29c.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE88720
Gene expression data from meningioma samples and healthy meningial cell line
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Although meningioma is a common disease, there is a lack of understanding of the underlying molecular mechanisms behind its initiation and progression. We used combined miRNA-mRNA transcriptome analysis to discover novel genes and networks in meningiomas.

Publication Title

Simultaneous analysis of miRNA-mRNA in human meningiomas by integrating transcriptome: A relationship between PTX3 and miR-29c.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE86036
Expression data from LIF treated chordoma cell lines U-CH1 and MUG-Chor1
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Leukemia Inhibitory Factor is an important cytokine of the IL family. Recent findings suggest it has a crucial role in cancer progression

Publication Title

Leukemia Inhibitory Factor Promotes Aggressiveness of Chordoma.

Sample Metadata Fields

Cell line

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accession-icon SRP049773
Effects of narciclasine treatment on major metabolic organs of C57BL/6 mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To test the effects of narciclasine treatment on major metabolic organs of C57BL/6 mice, we first fed the mice with a high fat diet (HFD) then gavaged them with the narciclasine weekly. After 7 weeks of narciclasine treatment, the four major metabolic organs WAT, BAT, Liver and muscle were harvested and the total RNA was prepared for RNA sequencing analysis. By analyzing the RNA-seq data sets, we found that the primary target of this narciclasine is skeletal muscle. Overall design: Examinaton of expression profile upon narciclasine trearment on different tissues

Publication Title

Narciclasine attenuates diet-induced obesity by promoting oxidative metabolism in skeletal muscle.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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