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accession-icon SRP125179
Natural Killer cells control tumor growth by sensing a growth factor
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Many tumors produce platelet-derived growth factor (PDGF)-DD, which promotes cellular proliferation, epithelial-mesenchymal transition, stromal reaction, and angiogenesis through autocrine and paracrine PDGFRß signaling. By screening a secretome library, we found that the human immunoreceptor NKp44 encoded by NCR2 and expressed on natural killer (NK) cells and innate lymphoid cells recognizes PDGF-DD. PDGF-DD engagement of NKp44 triggered NK cell secretion of IFN-? and TNF-a that induced tumor cell growth arrest. A distinctive transcriptional signature of PDGF-DD-induced cytokines and the downregulation of tumor cell cycle genes correlated with NCR2 and greater survival in glioblastoma. NKp44 expression in mouse NK cells controlled the dissemination of tumors expressing PDGF-DD more effectively than control mice, an effect enhanced by blockade of the inhibitory receptor CD96 or CpG-oligonucleotide treatment. Thus, whilst cancer cell production of PDGF-DD supports tumor growth and stromal reaction, it concomitantly activates innate immune responses to tumor expansion. Overall design: RNAseq of NK cell and tumor cell samples in reponse to various stimuli

Publication Title

Natural Killer Cells Control Tumor Growth by Sensing a Growth Factor.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE107043
Effect of PDGF-Ddstimulation on human tonsil ILC1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The effect of PDGF-DD on the gene expression of human tonsil ILC1 is unknown. We used microarray to determine the transcriptional differences between unstimulated and PDGF-DD-stimulated human tonsil ILC1.

Publication Title

Natural Killer Cells Control Tumor Growth by Sensing a Growth Factor.

Sample Metadata Fields

Specimen part

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accession-icon GSE60716
Cell-Independent MicroRNA Biogenesis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cancer exosomes perform cell-independent microRNA biogenesis and promote tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP197580
Group 3 innate lymphoid cells mediate early protective immunity against Mycobacterium tuberculosis
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the phenotype of human lung ILC2 and ILC3 populations from individuals with tuberculosis (TB) and non-TB cancer controls. We find that ILC2s demonstrate moderate transcriptional differences in TB infection, whereas ILC3s demonstrate large differences. Overall design: ILC2s and ILC3s were purified by FACS from lung biopsies from TB infected lung tissue and peripheral healthy lung tissue from individuals with cancer. Low-input RNA-seq was performed on 1-3 replicates (dependent on cell number) on 5 individuals with TB infection and 2 controls.

Publication Title

Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon E-MEXP-137
Transcription profiling of mouse NIH3T3 cells transformed with oncovav2 deprived of Serum
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Effect of the overexpression of the oncogenic form of the Vav2 protein in the NIH3T3 cell line under serum deprivation conditions. oncovav2-transformed NIH3T3 cells grown in serum-deprived medium (Vav2SD) are compared to the parental NIH3T3 controls under the same growth conditions (ContSD). Vav2SD cells are also compared to the oncovav2-transformed NIH3T3 cells growing exponentially and the NIH3T3 growing exponentially.

Publication Title

Microarray analysis of gene expression with age in individual nematodes.

Sample Metadata Fields

Cell line

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accession-icon SRP158328
Leukodystrophy-associated POLR3A mutations down-regulate the RNA polymerase III transcript and important regulatory RNA BC200
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

RNA polymerase III (Pol III) is an essential enzyme responsible for the synthesis of several small non-coding RNAs, a number of which are involved in mRNA translation. Recessive mutations in POLR3A, encoding the largest subunit of Pol III, cause POLR3-related hypomyelinating leukodystrophy (POLR3-HLD), characterized by deficient central nervous system myelination. Identification of the downstream effectors of pathogenic POLR3A mutations has been so far elusive. Here, we used CRISPR-Cas9 to introduce the POLR3A mutation c.2554A>G (p.M852V) into human cell lines and assessed its impact on Pol III biogenesis, nuclear import, DNA occupancy, transcription, and protein levels. Transcriptomic profiling uncovered a subset of transcripts vulnerable to Pol III hypofunction, including a global reduction in tRNA levels. The brain cytoplasmic BC200 RNA (BCYRN1), involved in translation regulation, was consistently affected in all our cellular models, including patient-derived fibroblasts. Genomic BC200 deletion in an oligodendroglial cell line led to major transcriptomic and proteomic changes, having a larger impact than those of POLR3A mutations. Upon differentiation, mRNA levels of the MBP gene, encoding myelin basic protein, were significantly decreased in POLR3A-mutant cells. Our findings provide the first evidence for impaired Pol III transcription in cellular models of POLR3-HLD and identify several candidate effectors, including BC200 RNA, having a potential role in oligodendrocyte biology and involvement in the disease. Overall design: Gene expression profiling of Pol III transcripts in control and POLR3A-mutated cell lines (HEK293 and MO3.13) using RNA-seq and small RNA-seq; ChIP-seq of FLAG-tagged POLR3A-WT and mutated POLR3A-M852V

Publication Title

Leukodystrophy-associated <i>POLR3A</i> mutations down-regulate the RNA polymerase III transcript and important regulatory RNA <i>BC200</i>.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE59453
Transcriptomic changes in the duodenum mucosa after a high-fat (HF) or low-fat (LF) meal ingestion.
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Fat intake is an important determinant in the development of obesity. The small intestine is the principal site of digestion and absorption of nutrients, and these short-term circulating nutrients and hormones as well as neural signals derived from the peripheral tissues in responses to a meal act at multiple central nervous system sites where food intake is controlled.

Publication Title

Identification of the principal transcriptional regulators for low-fat and high-fat meal responsive genes in small intestine.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP067226
The LIM homeodomain transcription factor Lhx2 is required for Müller glia development in the vertebrate retina.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: Müller glia are the only glial cell type produced by the neuroepithelial progenitor cells which generate the vertebrate retina. Müller glia are required to maintain retinal homeostasis and support the survival of retinal neurons. Furthermore, they function as an adult stem cell, mediating retinal regeneration among select vertebrate classes. However, the mechanisms which regulate Müller development are poorly understood as considerable overlap exists in gene expression between retinal progenitor cells and differentiated Müller glia. We investigate the functional role of the LIM homeodomain transcription factor Lhx2 in the specification and development of Müller glia in the mouse. Methods: RNA-Seq was performed in collaboration with the Johns Hopkins School of Medicine Deep Sequencing and Microarray Core Facility. Libraries were prepared using Illumina TruSeq RNA Sample kit (Illumina, San Diego, CA) following manufacturer’s recommended procedure. The PCR amplified library was purified using RNAClean XP magnetic beads (Agencourt, Beverley, MA) and run out on a High Sensitivity DNA Chip (Agilent, Santa Clara, CA) for quality check. We used STAR to align RNA-Seq reads onto Ensembl mouse genome GRCm38, release 72. To generate the stand attribute for alignments containing splice junctions, we used the outSAMstrandField intronMotif program. The spliced alignments without strand definition were removed. Number of reads mapped to exons was counted by htseq-count. Genes expressed at very low levels were omitted from further analysis. Gene expression differences between wildtype and mutant samples, significance (p-value) and false discovery rate (FDR) were computed using the generalized linear models based EdgeR. Results: We observed a substantial reduction in expression of Notch pathway genes including Notch1, the Notch ligands Dll1 and Dll3, as well as gliogenic Notch effector genes such as Hes1, Hes5, Id1 and Sox8 and the Müller-gliogenic factor Rax. We likewise observe a substantial reduction in expression of progenitor-specific genes such as Vsx2 and Fgf15. Furthermore, we observed a decrease in the expression of early-onset glial markers such as Crym , Spon1, and Car2. Overall design: Retinal mRNA profiles of post-natal day 0.5 (P0.5) Lhx2 wild type (N=3) and Lhx2lox/lox; Pdgfra-Cre ?cKO (N=3) mice were generated using Illumina TruSeq and analyzed with Agilent high sensitivity DNA analsis kit.

Publication Title

Lhx2 Is an Essential Factor for Retinal Gliogenesis and Notch Signaling.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP074580
Macrophage Colony Stimulating Factor derived from CD4+ T cells aids in control of an intracellular infection [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Background: In malaria, parasites of the genus Plasmodium elicit robust host expansion of macrophages and monocytes, but the underlying mechanisms remain unclear. In a microarray analysis of pooled, activated CD4+ T cells from mice infected with P. chabaudi, we detected inducible expression of Csf1, which promotes macrophage proliferation. To better characterize Csf1-producing T cells, single-cell RNA-Seq was performed. Results: Robust Csf1 expression was detected in a subset of sampled CD4+ T cells (n = 14/35), whereas the remainder of cells had no detectable Csf1. Further, we identified ~ 400 genes that were differentially expressed between Csf1+ and Csf1- T cells. Conclusions: This work defines the transcriptional landscape of a subset of activated CD4+ T cells that produce the cytokine Csf1. These cells are expected to be important in infections with intracellular pathogens such as Plasmodium. Overall design: Antigen-experienced (CD11a+ CD49d+) CD4+ T cells were isolated by double-sorting from the blood of C57BL/6 adult female mice 6 days post-infection with Plasmodium chabaudi. Single cells were isolated and processed for RNA sequencing using a Fluidigm C1 integrated fluidic circuit chip. 35 biological replicates were analyzed.

Publication Title

Macrophage Colony Stimulating Factor Derived from CD4+ T Cells Contributes to Control of a Blood-Borne Infection.

Sample Metadata Fields

Sex, Specimen part, Subject, Time

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accession-icon GSE44246
Human foreskin fibroblasts (HFFs) infected with type I strains of Toxoplasma gondii
  • organism-icon Toxoplasma gondii, Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genetic basis for phenotypic differences between different Toxoplasma gondii type I strains.

Sample Metadata Fields

Specimen part, Treatment

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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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