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accession-icon SRP171981
Gender-specific transcriptomic changes with high fat diet
  • organism-icon Drosophila melanogaster
  • sample-icon 181 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

we investigated the effect of HFD on the transcriptome in the heads and bodies of male and female flies kept on either HFD or regular diet (RD). Using comprehensive genomic analyses which include high-throughput transcriptome sequencing, pathway enrichment and gene network analyses, we found that HFD induces a number of responses that are sexually dimorphic in nature. There was a robust transcriptional response consisting of a downregulation of stress-related genes in the heads and glycoside hydrolase activity genes in the bodies of males. In the females, the HFD led to an increased transcriptional change in lipid metabolism. Overall design: Examination of head and body of male and female Drosophila kept on High fat and regular diet.

Publication Title

High fat diet induces sex-specific differential gene expression in Drosophila melanogaster.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE37012
Gene expression profiling upon knockdown of JAK1 in IM9 cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Natural Killer (NK) cells are primary effectors of innate immunity directed against transformed cells. In response, tumor cells have developed mechanisms to evade NK cell-mediated lysis but the molecular basis for target cell resistance is not well understood. In the present study, we used a lentiviral shRNA library targeting more than 1000 human genes to identify 83 genes that promote target cell resistance to human NK cells. Many of the genes identified in this genetic screen belong to common signaling pathways, however, none of these genes have previously been known to modulate susceptibility of human tumor cells to immunologic destruction. In particular, gene silencing of two members of the JAK family (JAK1 and JAK2) in a variety of tumor cell targets increased their susceptibility to NK-mediated lysis and induced increased secretion of interferon gamma (IFN-gamma by NK cells. Treatment of tumor cells with JAK inhibitors also induced increased susceptibility to NK cell activity. These findings may have important clinical implications and suggest that small molecule inhibitors of tyrosine kinases being developed as therapeutic anti-tumor agents may also have significant immunologic effects in vivo.

Publication Title

Tyrosine kinase pathways modulate tumor susceptibility to natural killer cells.

Sample Metadata Fields

Cell line

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accession-icon GSE21373
Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence
  • organism-icon Staphylococcus aureus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix S. aureus Genome Array (saureus)

Description

Staphylococcus aureus is a major human pathogen and resistant to numerous clinically used antibiotics. The first antibiotic developed for S. aureus infections was the nonribosomal petide secondary metabolite penicillin. We discovered cryptic nonribosomal peptide secondary metabolites, the aureusimines, made by S. aureus itself that are not antibiotics, but function as small molecule regulators of virulence factor expression. Using established rules and codes for nonribosomal peptide assembly we predicted these nonribosomal peptides, and used these predictions to identify them from S. aureus culture broths. Functional studies using global microarray and mouse bacteremia models established that the aureusimines control virulence factor expression and are necessary for productive infections. This is the first report of the aureusimines and has important implications for the treatment of drug resistant S. aureus. Targeting aureusimine synthesis may provide novel anti-infectives.

Publication Title

Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP125739
Expression levels of genes of LCMV.GP66-77 specific CD4 T cells isolated from bone marrow (BM) and spleen, 3 days after antigenic re-challenge
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed RNA-Seq and compared expression levels of genes of reactivated LCMV.GP66-77 specific CD4 T cells isolated from bone marrow (BM) and spleen of LCMV.GP61-80 primed C57BL/6 mice. Cells were isolated 3 days after antigenic re-challenge Overall design: C57BL/6 mice were primed at day 0 with LCMV.GP61-80-NP-MSA + poly(I:C) and immunized again at day 14 with LCMV.GP61-80 + poly(I:C). 60 days later, C57BL/6 mice were boosted with LCMV.GP61-80-NP-MSA + poly(I:C) and 3 days after the boost, LCMV specific CD4 T cells were isolated from BM and spleen

Publication Title

Nonfollicular reactivation of bone marrow resident memory CD4 T cells in immune clusters of the bone marrow.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE54169
Differential regulation patterns of anti-CD20 mAbs in MCL
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We investigated the differential regulation patterns of type I anti-CD20 monoclonal antibody (mAb) rituximab and type II obinutuzumab on a transcriptional level. Using a panel of MCL cell lines, we determined the effects of obinutuzumab and rituximab as monotherapies as well as in combination on cell viability and proliferation.

Publication Title

Differential regulation patterns of the anti-CD20 antibodies obinutuzumab and rituximab in mantle cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE43401
MYBL2 Is a Sub-haploinsufficient Tumor Suppressor Gene in Myeloid Malignancy
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MYBL2 is a sub-haploinsufficient tumor suppressor gene in myeloid malignancy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE43399
MYBL2 Is a Sub-haploinsufficient Tumor Suppressor Gene in Myeloid Malignancy (RNA)
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A dosage-dependent role for tumor suppressor genes in the initiation of myeloid malignancies remains controversial. Here we show that MYBL2 is expressed at sharply reduced levels in CD34+ cells from most patients with myelodysplastic syndrome (MDS; 65%; n=26). In a murine competitive reconstitution model, Mybl2 knockdown by RNAi to 20-30% of normal levels in multipotent hematopoietic progenitors led to clonal dominance by these sub-haploinsufficient cells, affecting all blood cell lineages. By 6 months post-transplantation, the reconstituted mice had developed a myeloproliferative/myelodysplastic disorder originating from the cells with aberrantly reduced Mybl2 expression. Thus, downregulation of MYBL2 activity to levels below those predicted by classical haploinsufficiency drives the clonal expansion of hematopoietic progenitors in a large fraction of human MDS cases.

Publication Title

MYBL2 is a sub-haploinsufficient tumor suppressor gene in myeloid malignancy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE43400
MYBL2 Is a Sub-haploinsufficient Tumor Suppressor Gene in Myeloid Malignancy (RNAi)
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A dosage-dependent role for tumor suppressor genes in the initiation of myeloid malignancies remains controversial. Here we show that MYBL2 is expressed at sharply reduced levels in CD34+ cells from most patients with myelodysplastic syndrome (MDS; 65%; n=26). In a murine competitive reconstitution model, Mybl2 knockdown by RNAi to 20-30% of normal levels in multipotent hematopoietic progenitors led to clonal dominance by these sub-haploinsufficient cells, affecting all blood cell lineages. By 6 months post-transplantation, the reconstituted mice had developed a myeloproliferative/myelodysplastic disorder originating from the cells with aberrantly reduced Mybl2 expression. Thus, downregulation of MYBL2 activity to levels below those predicted by classical haploinsufficiency drives the clonal expansion of hematopoietic progenitors in a large fraction of human MDS cases.

Publication Title

MYBL2 is a sub-haploinsufficient tumor suppressor gene in myeloid malignancy.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP158475
Transcriptome analysis of antigen-specific T follicular helper (Tfh) cells and non-Tfh cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

To identify transcription factors critically involved in the Tfh cell transcriptional network, antigen-specific Tfh and non-Tfh cells from a day 8 immune response were analyzed by RNA-seq. Overall design: Ovalbumin-specific T cells from OT-II TCR-transgenic mice were transferred into C57BL/6 recipients, which were immunized subcutaneously with nitrophenol coupled to ovalbumin. Eight days after immunization, transgenic T cells from pooled inguinal lymph nodes were sorted for a CD44hi CXCR5+ PD-1+ Tfh and CD44hi CXCR5- PD-1- non-Tfh cell phenotype for analysis by RNA-seq.

Publication Title

Bach2 Controls T Follicular Helper Cells by Direct Repression of Bcl-6.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP198678
Single-Cell transcriptomes of murine Bone Marrow Stromal Cells Reveal Niche-Associated Heterogeneity
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconNextSeq 500

Description

Bone marrow (BM) stromal cells are important in the development and maintenance of cells of the immune system. Using single cell RNA sequencing, we here explore the functional and phenotypic heterogeneity of individual transcriptomes of 1,167 murine BM mesenchymal stromal cells. These cells exhibit a tremendous heterogeneity of gene expression, which precludes the identification of defined subpopulations. However, according to the expression of 108 genes involved in the communication of stromal cells with hematopoietic cells, we have identified 14 non-overlapping subpopulations, with distinct cytokine or chemokine gene expression signatures. With respect to the maintenance of subsets of immune memory cells by stromal cells, we identify distinct subpopulations expressing IL7, IL15 and Tnfsf13b. Together, this study provides a comprehensive dissection of the BM stromal heterogeneity at the single cell transcriptome level and provides a basis to understand their lifestyle and their role as organizers of niches for the long-term maintenance of immune cells. Overall design: For single cell library preparation, ex vivo FACS sorted VCAM-1+CD45-Ter119-CD31- BM cells were applied to the 10X Genomics platform using the Single Cell 3' Reagent Kit V2 (10x Genomics) following the manufacturer's instructions. Upon adapter ligation and index PCR, the quality of the obtained cDNA library was assessed by Qubit quantification, Bioanalyzer fragment analysis (HS DNA Kit, Agilent) and KAPA library quantification qPCR (Roche). The sequencing was performed on a NextSeq500 device (Illumina) using a High Output v2 Kit (150 cycles) with the recommended sequencing conditions (read1: 26nt, read2: 98nt, index1: 8 nt, index2: n.a.).

Publication Title

Single-cell transcriptomes of murine bone marrow stromal cells reveal niche-associated heterogeneity.

Sample Metadata Fields

Specimen part, Subject

View Samples
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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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