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accession-icon GSE95364
Dysregulated gene expression in cardiac chambers of adult Mef2a knockout mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In this study, we have identified MEF2A-sensitive genes in atrial and ventricular chambers of the adult heart. MEF2A is a member of the myocyte enhancer factor 2 (MEF2) family of transcription factors. MEF2 proteins are expressed in skeletal and cardiac muscle tissues and are conserved across many mammalian species, but the gene programs regulated by MEF2A in adult cardiac chambers are largely unknown. We compared gene expression profiles between WT and Mef2a knockout atria and ventricles from adult mice, and the results identified distinct and overlapping sets of genes sensitive to the loss of MEF2A in the adult heart.

Publication Title

The transcription factor MEF2A fine-tunes gene expression in the atrial and ventricular chambers of the adult heart.

Sample Metadata Fields

Specimen part

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accession-icon SRP093643
Allelic expression in tibial growth plates from 21 day old C57BL/6J x CAST/EiJ F1s
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We have identified candidate genes from the Feml2 QTL influencing femur length through allele specific expression analysis of growth plates in C57BL/6J x CAST/EiJ F1 hybrids. This work provides the foundation to identify novel genes affecting bone geometry. Overall design: total RNA sequencing in 7 male C57BL/6JxCAST F1s

Publication Title

Genetic Dissection of a QTL Affecting Bone Geometry.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE58274
Mouse ureter: wild type vs miR-143/145 knock out
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis

Publication Title

Deletion of the miR-143/145 cluster leads to hydronephrosis in mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE55838
Mouse isolated kidney preglomerular arterioles: wild type vs conditional knockout of RBP-J in renin cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

mRNA profiling of mouse kidney preglomerular arterioles comparing wild type arterioles vs.arterioles from mice having deletion of RBP-J in cells of the renin lineage

Publication Title

Recombination signal binding protein for Ig-κJ region regulates juxtaglomerular cell phenotype by activating the myo-endocrine program and suppressing ectopic gene expression.

Sample Metadata Fields

Sex, Age

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accession-icon GSE53916
Expression data from mouse bone marrow cells expressing renin driven expression of green fluorescent protein.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Local renin antiotensin systems have been identified for many extra-renal sites. Bone marrow has been proposed as one such site, although the nature of the renin-expressing cell type(s) has not been established.

Publication Title

Identification of renin progenitors in the mouse bone marrow that give rise to B-cell leukaemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE46229
Mouse spleen: wild type vs leukemic
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia

Publication Title

Identification of renin progenitors in the mouse bone marrow that give rise to B-cell leukaemia.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon SRP108664
Whole larvae and nociceptive neuron RNA-Seq samples
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study was to identify ion channels, specifically transient receptor potential cation channel A (trpA1) channels, that were highly expressed and enriched in nociceptive sensory neurons of Drosophila larvae. In class IV da sensory neurons, we find that TrpA1 is the most highly expressed trpA1 channel of the 14 trpA1 channels in Drosophila, and that its expression is highly enriched when compared to the whole animal transcriptome. Overall design: Four biological replicates of 100 Drosophila melanogaster larval class IV dendritic arborization sensory neurons and five biological replicates of whole Drosophila melanogaster larvae were profiled by mRNA-Seq

Publication Title

TrpA1 activation in peripheral sensory neurons underlies the ionic basis of pain hypersensitivity in response to vinca alkaloids.

Sample Metadata Fields

Subject

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accession-icon SRP159400
High Dimensional Analysis Delineates Myeloid and Lymphoid Compartment Remodeling during Successful Immune Checkpoint Cancer Therapy
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Using complementary forms of high dimensional profiling we define differences in CD45+ cells from syngeneic mouse tumors that either grow progressively or eventually reject following immune checkpoint therapy (ICT). Unbiased assessment of gene expression of tumor infiltrating cells by single cell RNA sequencing (scRNAseq) and longitudinal assessment of cellular protein expression by mass cytometry (CyTOF) revealed significant remodeling of both the lymphoid and myeloid intratumoral compartments. Surprisingly, we observed multiple subpopulations of monocytes/macrophages distinguishable by the combinatorial presence or absence of CD206, CX3CR1, CD1d and iNOS, markers of different macrophage activation states that change over time during ICT in a manner partially dependent on IFN?. Both the CyTOF data and additional analysis of scRNAseq data support the hypothesis that macrophage polarization/activation results from effects on circulatory monocytes/early macrophages entering tumors rather than on pre-polarized mature intratumoral macrophages. Thus, ICT induces transcriptional and functional remodeling of both myeloid and lymphoid compartments. Overall design: Droplet-based 3' end massively parallel single-cell RNA sequencing was performed by encapsulating sorted live CD45+ tumor infiltrating cells into droplets and libraries were prepared using Chromium Single Cell 3' Reagent Kits v1 according to manufacturer's protocol (10x Genomics). The generated scRNAseq libraries were sequenced using an Illumina HiSeq2500.

Publication Title

High-Dimensional Analysis Delineates Myeloid and Lymphoid Compartment Remodeling during Successful Immune-Checkpoint Cancer Therapy.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP062238
Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Left ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. Overall design: RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.

Publication Title

Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE61692
Expression data from OVCAR-3 cells overexpressing histone H1.3
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Ovarian cancer is a deadly gynecological malignancy for which novel biomarkers and therapeutic targets are imperative for improving survival. To investigate the role of histone H1 in ovarian cancer cells, we overexpress a histone H1 variant, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line. RNA was extracted from OV-3/H1.3(H) cells (OVCAR-3 with overexpression of H1.3) and control cells of OVCAR-3 transfected with vectors without H1.3. The microarray chip used was human Affymetrix ST1.0 array. Gene expression changes caused by overexpression of H1.3 in OVCAR-3 cells were identified.

Publication Title

Histone h1.3 suppresses h19 noncoding RNA expression and cell growth of ovarian cancer cells.

Sample Metadata Fields

Specimen part, Cell line

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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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