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accession-icon GSE13506
Galanin preproprotein is associated with elevated plasma triglycerides
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Assessment of mRNA expression levels in fat biopsies from subcutaneous adipose tissue from unrelated individuals.

Publication Title

Galanin preproprotein is associated with elevated plasma triglycerides.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17170
A systems genetics approach implicates USF1, FADS3 and other causal candidate genes for familial combined hyperlipidemia
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Assessment of mRNA expression levels in fat biopsies from subcutaneous adipose tissue from unrelated individuals.

Publication Title

A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE17300
Overexpression of USF1 in HEK293T cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Overexpression of USF1 in HEK293T cells in vitro to ascertain the genes downstream of USF1. Will identify direct targets as well as indirect targets of USF1.

Publication Title

A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.

Sample Metadata Fields

Cell line

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accession-icon SRP049719
ELAVL1 modulates transcriptome-wide miRNA binding in murine macrophages
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Post-transcriptional gene regulation by miRNAs and RNA binding proteins (RBP) is important in development, physiology and disease. To examine the interplay between miRNAs and the RBP ELAVL1 (a.k.a. HuR), we mapped miRNA binding sites on a transcriptome-wide scale in WT and Elavl1 knockout murine bone marrow-derived macrophages. Proximity of ELAVL1 binding sites attenuated miRNA binding to transcripts and promoted gene expression. Transcripts that regulate angiogenesis and macrophage/ endothelial cross talk were preferentially targeted by miRNAs, suggesting that ELAVL1 promotes angiogenesis, at least in part, by antagonism of miRNA function. We found that ELAVL1 antagonized binding of miR-27 to the 3'UTR of Zfp36 mRNA and alleviated miR-27-mediated suppression of the RBP ZFP36 (a.k.a. Tristetraprolin). Thus the miR-27-regulated mechanism synchronizes the expression of ELAVL1 and ZFP36. This study provides a resource for systems-level interrogation of post-transcriptional gene regulation in macrophages, a key cell type in inflammation, angiogenesis and tissue homeostasis. Overall design: Bone marrow derived macrpohges mRNA profiles of 7-day cultured wild type (WT) and Elavl1l-/- mouse bone marrow cells were generated by deep sequencing, with 4 biologic duplication, using Illumina GAII.

Publication Title

ELAVL1 modulates transcriptome-wide miRNA binding in murine macrophages.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP145350
A distinct lineage of origin reveals heterogeneity of plasmacytoid dendritic cells III
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Plasmacytoid  dendritic cells (pDCs) are an immune subset devoted to the production of high amounts of type 1 interferons in response to viral infections. While conventional dendritic cells (cDCs) originate mostly from a common dendritic cell progenitor (CDP), pDCs have been shown to develop from both CDPs and common lymphoid progenitors (CLP). Here we found that pDCs developed predominantly from IL7R+ lymphoid progenitor cells. Expression of SiglecH and Ly6D  defined pDC lineage commitment along the lymphoid branch. Transcriptional characterization of SiglecH+Ly6D+ precursors indicated that pDC development requires high expression of the transcription factor IRF8, while pDC identity relies on TCF4. RNA sequencing of IL7R+ lymphoid and CDP-derived pDCs mirrored the heterogeneity of mature pDCs observed by single-cell analysis. Both mature pDC subsets are able to secrete type 1 interferons, but only myeloid-derived pDCs share with cDCs their ability to process and present antigen. Overall design: Bulk RNA Seq was performed from sort purified DN, SP and DP lymphoid progenitors and BM pDCs of 4 individual mice

Publication Title

Distinct progenitor lineages contribute to the heterogeneity of plasmacytoid dendritic cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP145346
A distinct lineage of origin reveals heterogeneity of plasmacytoid dendritic cells II (scRNAseq)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Plasmacytoid  dendritic cells (pDCs) are an immune subset devoted to the production of high amounts of type 1 interferons in response to viral infections. While conventional dendritic cells (cDCs) originate mostly from a common dendritic cell progenitor (CDP), pDCs have been shown to develop from both CDPs and common lymphoid progenitors (CLP). Here we found that pDCs developed predominantly from IL7R+ lymphoid progenitor cells. Expression of SiglecH and Ly6D  defined pDC lineage commitment along the lymphoid branch. Transcriptional characterization of SiglecH+Ly6D+ precursors indicated that pDC development requires high expression of the transcription factor IRF8, while pDC identity relies on TCF4. RNA sequencing of IL7R+ lymphoid and CDP-derived pDCs mirrored the heterogeneity of mature pDCs observed by single-cell analysis. Both mature pDC subsets are able to secrete type 1 interferons, but only myeloid-derived pDCs share with cDCs their ability to process and present antigen. Overall design: BM and splenic pDCs were sorted from 3 mice and 3000 cells/sample were used for single cell RNA Seq (10x genomics)

Publication Title

Distinct progenitor lineages contribute to the heterogeneity of plasmacytoid dendritic cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP076270
Comparison of human brain and spinal cord neural stem cells (NSCs)
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Regional identity of several kind of human neural stem cells were assessed by RNA-Seq Overall design: We compared whole transcriptome of human fetal spinal cord, fetal brain, fetal spinal cord derived NSCs, H9-derived NSCs, H9-derived spinal cord NSCs, and UCSF4-derived spinal cord NSCs

Publication Title

Generation and post-injury integration of human spinal cord neural stem cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE10960
Strand-specific 5'-O-methylation of siRNA duplexes controls guide strand selection and targeting specificity.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Small interfering RNAs (siRNAs) and microRNAs (miRNAs) guide catalytic sequence-specific cleavage of fully or nearly fully complementary target mRNAs or control translation and/or stability of many mRNAs that share 6-8 nucleotides (nt) of complementarity to the siRNA and miRNA 5' end. siRNA- and miRNA-containing ribonucleoprotein silencing complexes are assembled from double-stranded 21- to 23-nt RNase III processing intermediates that carry 5' phosphates and 2-nt overhangs with free 3' hydroxyl groups. Despite the structural symmetry of a duplex siRNA, the nucleotide sequence asymmetry can generate a bias for preferred loading of one of the two duplex-forming strands into the RNA-induced silencing complex (RISC). Here we show that the 5'-phosphorylation status of the siRNA strands also acts as an important determinant for strand selection. 5'-O-methylated siRNA duplexes refractory to 5' phosphorylation were examined for their biases in siRNA strand selection. Asymmetric, single methylation of siRNA duplexes reduced the occupancy of the silencing complex by the methylated strand with concomitant elimination of its off-targeting signature and enhanced off-targeting signature of the phosphorylated strand. Methylation of both siRNA strands reduced but did not completely abolish RNA silencing, without affecting strand selection relative to that of the unmodified siRNA. We conclude that asymmetric 5' modification of siRNA duplexes can be useful for controlling targeting specificity.

Publication Title

Strand-specific 5'-O-methylation of siRNA duplexes controls guide strand selection and targeting specificity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3425
Silencing of microRNAs in vivo with "antagomirs"
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Using a novel class of chemically-engineered oligonucleotides, termed "antagomirs", we studied the biological significance of silencing miR-122 in the liver of mice at the mRNA level

Publication Title

Silencing of microRNAs in vivo with 'antagomirs'.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE85173
Graded responses to variable TCR signaling are encoded in the affinities of AICE-containing enhancers responding to BATF and IRF4 [gene expression]
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Variable strengths of T cell receptor (TCR) signaling can produce divergent outcomes for T cell development and function. The mechanisms leading to different outcomes are incompletely understood, but may include distinct activation thresholds for different transcription factors as well as distinct sensitivities among target genes to transcription factors. IRF4 is one transcription factor implicated in responses to variable TCR signal strength. IRF4 expression increases uniformly with increasing TCR signal strength (i.e., analog), but it is unclear how IRF4 induced distinct genes at different levels, rather than different amounts of the same genes. Here, we analyzed global gene expression in TH2 cells and used ChIP-seq to define the relationship between TCR signal strength, enhancer occupancy and transcriptional activity for BATF/IRF4-dependent genes. We show that enhancers exhibit a spectrum of affinity for the BATF/IRF4 ternary complex mediate graded responsiveness of individual genes to increasing TCR signal strength. Differential gene induction by BATF and IRF4 occurs through interaction with enhancer elements of different affinity for BATF/IRF4 complexes. The increased resolution of factor binding site identified using ChIP-exo allowed the identification of a novel AICE2 motif binding BATF/IRF4 with higher affinity and that this may explain the protective role of a single nucleotide polymorphism in the CTLA-4 locus known to decrease the incidence of autoimmune diseases.

Publication Title

Quality of TCR signaling determined by differential affinities of enhancers for the composite BATF-IRF4 transcription factor complex.

Sample Metadata Fields

Specimen part

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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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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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