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accession-icon GSE3788
Lin-, CD38-, CD34+ Hematopoietic Stem Cells.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Lin-, CD38-, CD34+ hematopoietic stem cells.

Publication Title

Microarray and serial analysis of gene expression analyses identify known and novel transcripts overexpressed in hematopoietic stem cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE10556
Comparision of expression profile between wild-type and Slc39a13 knockout chondrocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In order to explore molecules whose expression is controlled by Slc39a13, we investigated gene expression profiling of primary chondrocyte isolated from wild-type and Slc39a13 knockout mice.

Publication Title

The zinc transporter SLC39A13/ZIP13 is required for connective tissue development; its involvement in BMP/TGF-beta signaling pathways.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10555
Comparision of expression profile between wild-type and Slc39a13 knockout osteoblasts
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In order to explore molecules whose expression is controlled by Slc39a13, we investigated gene expression profiling of primary osteoblast isolated from wild-type and Slc39a13 knockout mice.

Publication Title

The zinc transporter SLC39A13/ZIP13 is required for connective tissue development; its involvement in BMP/TGF-beta signaling pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP059205
Landscape of Hematopoiesis Described in Induced Pluripotent Stem Cells and Human Bone Marrow
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Granulopoietic differentiation of myeloid progenitor cells derived from control iPSCs was performed in a two-step liquid culture. At the end of culture, stages of differentiation were identified by morphological analysis and submitted for RNA-sequencing analysis in order to provide insight into the genomic landscape of myeloid lineage hematopoiesis as modeled by the in vitro induced differentiation of iPSCs as compared to in vivo bone marrow-derived promyelocytes. Overall design: Peripheral blood from healthy controls was obtained and iPSC were generated from peripheral blood mononuclear cells. Hematopoietic progenitors generated from control iPSCs when cultured in myeloid expansion medium containing 50ng/mL SCF, 10ng/mL IL-3 and 10ng/mL GM-CSF for 5 days at which point cells were stained for CD45-Pacific blue, CD34-PECy7, CD33-AP, CD11b-APC-Cy7, CD15-FITC. 7-AAD was used to eliminate the dead cells. The promyelocytic population (CD45+CD34-CD33+CD11b-CD15+/lo) was sorted and the RNA from control iPSC promyelocytes was isolated using QIAGEN RNAeasy mini kit. The RNA samples were processed for RNA-seq analyses using RNA-seq protocol from NuGEN and Illumina. The amplified products were sequenced to analyze the gene expression profile of each replicate sample. A total of 20 samples were used in this analysis to characterize and compare iPSC in vitro differentiated myeloid cells with those isolated from human bone marrow.

Publication Title

p62 is required for stem cell/progenitor retention through inhibition of IKK/NF-κB/Ccl4 signaling at the bone marrow macrophage-osteoblast niche.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE48558
Expression data from normal and Malignant hematopoietic cells
  • organism-icon Homo sapiens
  • sample-icon 170 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This data was used to determine levels of BRCA1 and BRCA2 in primary human leukemia samples. Samples were determined to be high BRCA1 and/or BRCA2 or low BRCA1 and/or BRAC2.

Publication Title

Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE47927
Comparing gene expression in stem/progenitor cells from patients with CML in chronic, accelerated and blastic phase with normal volunteers
  • organism-icon Homo sapiens
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A comparison of global gene expression between rigorously defined stem and progenitor cells from patients with chronic myeloid leukaemia (CML) in chronic (CP), accelerated (AP) and blastic (BC) phase and similar populations isolated from normal volunteers.

Publication Title

Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

View Samples
accession-icon GSE24183
Genomic profiling of enzastaurin-treated B cell lymphoma RL cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Follicular lymphoma (FL) is an indolent lymphoma associated with follicular center B cells, and typically contains the Bcl-2 chromosomal translocation t(14;18), which leads to overexpression of the anti-apoptotic intracellular protein Bcl-2. FLs are sensitive to chemotherapy; however, patient relapses occur and response duration becomes progressively shorter, with the majority of patients eventually dying from the disease. Enzastaurin (LY317615), an acyclic bisindolylmaleimide, was initially developed as an ATP-competitive selective inhibitor of PKC. We found, in agreement with recent reports, that enzastaurin inhibits cell proliferation and induces apoptosis. These results are consistent with decreased phosphorylation of the Akt pathway and its downstream targets. To provide new insights into the anti-tumor action of enzastaurin on non-Hodgkin lymphoma, we investigated its effects on gene expression profiles of the B cell lymphoma RL cell line by oligonucleotide microarray analysis. We identified a set of 41 differentially expressed genes, mainly involved in cellular adhesion, apoptosis, inflammation, and immune and defense responses. These observations provide new insights into the mechanisms involved in the induction of apoptosis by enzastaurin in B cell lymphoma cell lines, and identify possible pathways that may contribute to the induction of apoptosis.

Publication Title

Genomic profiling of enzastaurin-treated B cell lymphoma RL cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon SRP038964
Systematic Mapping of ADAR1 Binding Reveals its Regulatory Roles in Multiple RNA Processing Pathways [small RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

ADARs are the primary factors underlying A-to-I editing in metazoans. We conducted the first global study of ADAR1-RNA interaction in human cells using CLIP-Seq. In contrast to the expected predominant binding of ADAR1 to Alu repeats, thousands of CLIP sites were located in non-Alu regions. This unexpectedly frequent non-Alu binding enabled discovery of transcriptome-wide functional and biophysical targets of ADAR1 in the regulation of mRNA processing including alternative 3'' UTR usage and alternative splicing. In addition, a global analysis of ADAR1 binding to non-Alu regions also revealed its primary interaction with microRNA (miRNA) transcripts in the nucleus, which subsequently affected expression levels of mature miRNAs. A complex global picture was revealed regarding the dependence of this function on the double-stranded RNA binding domains or deaminase activity. Our study unfolded a broad landscape of the diverse functional roles of ADAR1. Overall design: To identify ADAR binding dependent miRNA defferential expression profiles, U87MG cells were transfected with ADAR1 overexpression vector, RNA binding mutant (EAA and E912A), siRNA of ADAR1 or controls.

Publication Title

Genomic analysis of ADAR1 binding and its involvement in multiple RNA processing pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP038963
Systematic Mapping of ADAR1 Binding Reveals its Regulatory Roles in Multiple RNA Processing Pathways [CLIP-seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

ADARs are the primary factors underlying A-to-I editing in metazoans. We conducted the first global study of ADAR1-RNA interaction in human cells using CLIP-Seq. In contrast to the expected predominant binding of ADAR1 to Alu repeats, thousands of CLIP sites were located in non-Alu regions. This unexpectedly frequent non-Alu binding enabled discovery of transcriptome-wide functional and biophysical targets of ADAR1 in the regulation of mRNA processing including alternative 3'' UTR usage and alternative splicing. In addition, a global analysis of ADAR1 binding to non-Alu regions also revealed its primary interaction with microRNA (miRNA) transcripts in the nucleus, which subsequently affected expression levels of mature miRNAs. A complex global picture was revealed regarding the dependence of this function on the double-stranded RNA binding domains or deaminase activity. Our study unfolded a broad landscape of the diverse functional roles of ADAR1. Overall design: To charaterize ADAR1 binding profiles in U87 cells, we performed CLIP-seq using two different ADAR1 monoclonal antibodies.

Publication Title

Genomic analysis of ADAR1 binding and its involvement in multiple RNA processing pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP019272
Genetic regulation of human adipose microRNA expression and its consequences for metabolic traits
  • organism-icon Homo sapiens
  • sample-icon 362 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The genetics of messenger RNA expression has been extensively studied in humans and other organisms, but little is known about genetic factors contributing to microRNA (miRNA) expression. We examined natural variation of miRNA expression in adipose tissue in a population of 200 men who have been carefully characterized for metabolic syndrome phenotypes as part of the METSIM study. We genotyped the subjects using high-density SNP microarrays and quantified the mRNA abundance using genome-wide expression arrays and miRNA abundance using next generation sequencing. We reliably quantified 356 miRNA species that were expressed in human adipose tissue, a limited number of which made up most of the expressed miRNAs. We mapped the miRNA abundance as an expression quantitative trait and determined cis regulation of expression for 9 of the miRNAs and of the processing of one miRNA (miR-28). The degree of genetic variation of miRNA expression was substantially less than that of mRNAs. For the majority of the miRNAs, genetic regulation of expression was independent of the host mRNA transcript expression. We also showed that for 108 miRNAs, mapped reads displayed widespread variation from the canonical sequence. We found a total of 24 miRNAs to be significantly associated with metabolic syndrome traits. We suggest a regulatory role for miR-204-5p which was predicted to inhibit ACACB, a key fatty acid oxidation enzyme that has been shown to play a role in regulating body fat and insulin resistance in adipose tissue. Overall design: miRNA expression profiling of adipose tissue isolated from 200 humans

Publication Title

Genetic regulation of human adipose microRNA expression and its consequences for metabolic traits.

Sample Metadata Fields

Age, Specimen part, Subject

View Samples

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)

fund-icon Fund the CCDL

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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