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accession-icon GSE29144
Gene expression profiles after knockdown of Nardilysin in TMK-1 gastric cancer cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Nardilysin (NRDc), a metalloendopeptidase of the M16 family, has been reported to promote the ectodomain shedding and resulting activation of various growth factors and cytokines, but its role in cancer biology have not been elucidated.

Publication Title

Nardilysin and ADAM proteases promote gastric cancer cell growth by activating intrinsic cytokine signalling via enhanced ectodomain shedding of TNF-α.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP010940
Radicicol treatment of Drosophila cells
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Drosophila S2 cells were treated with Heat-shock protein 90 (Hsp90) inhibitor radicicol for 15min, 30min and 1h. Poly(A) RNA was isolated and sequenced. Overall design: Kinetics of transcriptional response to Hsp90 inhibition

Publication Title

Hsp90 globally targets paused RNA polymerase to regulate gene expression in response to environmental stimuli.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE66583
Expression profiles in Zbtb20-overexpressed neural precursor cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neural precursor cells (NPCs) are multipotent cells that can generate neurons, astrocytes, and oligodendrocytes in the mammalian central nervous system. Although Zbtb20 was expressed in NPCs, its functions in neural development are not fully understood. We performed microarray analysis to examine changes in gene expression between control and Zbtb20-overexpressed NPCs.

Publication Title

Zbtb20 promotes astrocytogenesis during neocortical development.

Sample Metadata Fields

Specimen part

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accession-icon GSE18361
Temporal gene expression analyisis from rice root (cv. Nipponbare) infected with Magnaporthe oryzae strain Guy11
  • organism-icon Oryza sativa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Magnaporthe oryzae causes rice blast, the most devastating foliar fungal disease of cultivated rice. During disease development the fungus simultaneously maintains both biotrophic and necrotrophic growth corresponding to a hemi-biotrophic life style. The ability of M. oryzae to also colonize roots and subsequently develop blast symptoms on aerial tissue has been recognized. The fungal root infection strategy and the respective host responses are currently unknown. Global temporal expression analysis suggested a purely biotrophic infection process reflected by the rapid induction of defense response-associated genes at the early stage of root invasion and subsequent repression coinciding with the onset of intracellular fungal growth. The same group of down-regulated defense genes was increasingly induced upon leaf infection by M. oryzae where symptom development occurs shortly post tissue penetration. Our molecular analysis therefore demonstrates the existence of fundamentally different tissue-specific fungal infection strategies and provides the basis for enhancing our understanding of the pathogen life style.

Publication Title

Tissue-adapted invasion strategies of the rice blast fungus Magnaporthe oryzae.

Sample Metadata Fields

Specimen part

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accession-icon SRP012463
Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

The Photo-Activatable Ribonucleoside-enhanced CrossLinking and ImmunoPrecipitation (PAR-CLIP) method was recently developed for global identification of RNAs interacting with proteins. The strength of this versatile method results from induction of specific T to C transitions at sites of interaction. However, current analytical tools do not distinguish between non-experimentally and experimentally induced transitions. Furthermore, geometric properties at potential binding sites are not taken into account. To surmount these shortcomings, we developed a two-step algorithm consisting of a non-parametric two-component mixture model and a wavelet-based peak calling procedure. Our algorithm can reduce the number of false positives up to 24% thereby identifying high confidence interaction sites. We successfully employed this approach in conjunction with a modified PAR-CLIP protocol to study the functional role of nuclear MOV10, a putative RNA helicase interacting with Argonaute2 and Polycomb. Our method, available as the R package wavClusteR, is generally applicable to any substitution-based inference problem in genomics. Overall design: The data comprises one MOV10 PAR-CLIP data file and one nuclear RNA-seq file

Publication Title

Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP090169
The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The molecular chaperone heat shock protein 90 (HSP90) is thought to buffer genetic variation uncoupling phenotypic outcome from individual genotypes. HSP90 thus acts as an evolutionary capacitor by facilitating an accumulation of natural genetic variation. The molecular mechanism underlying the buffering ability is unclear, and HSP90-contingent genetic variation maps both to coding and non-coding parts of the genome. Our genome-wide data indicate that a compromised chaperoning activity of HSP90 causes derepression of endogenous retroviruses (ERVs) in mouse somatic cells. This results in an upregulation of host genes located in the neighborhood of pre-existing ERVs insertion sites. We provide genetic and biochemical evidence that HSP90 cooperates with KAP1/ SETDB1 histone methyltranferase pathway to repress ERVs. Individual mouse strains have unique integration sites of ERVs in their genomes. Consequently distinct genes are responsive to HSP90 inhibitor in different mouse strains depending on the position of the genes vis-à-vis strain-specific ERV insertion sites. Since ERVs have been exapted to drive novel transcriptional networks during mammalian evolution, HSP90 may have acted as a capacitor by buffering variation caused by ERV in non-coding regions of the genome. Our studies provide the first molecular framework by which HSP90 can mitigate genetic variation in gene-regulatory regions affecting gene expression and phenotypes. Overall design: We have performed RNA-seq in mouse embryonic stem cells, neuronal progenitor cells and bone-marrow-derived macrophages treated with NVP-AUY922 in triplicates.

Publication Title

The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE11119
SOL2 mutation affect gene expresstion at root apex
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Analysis of sol2 mutant. SOL2 protein is a receptor-like kinase

Publication Title

The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP101840
Differential gene expression in MZudu v. WT zebrafish gastrulae
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We report RNA-sequencing data from zebrafish embryos lacking both maternal and zygotic expression of udu (which encodes Gon4l) (MZudu) at tailbud (TB) stage. Transcripts were compared to stage-matched wild-type (WT) embryos to identify differentially expressed genes. Overall design: Sequencing of polyadenylated mRNAs from MZudu mutant and control WT embryos with 2 biological and 2 technical replicates per genotype - each with 3 lanes per sample.

Publication Title

Gon4l regulates notochord boundary formation and cell polarity underlying axis extension by repressing adhesion genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10273
Convergent molecular pathways that induce immunoglobulin light-chain recombination
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle arrest and rearrangement of the kappa () or lambda () light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling. IRF-4 targets the 3 and enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells.

Publication Title

Regulation of immunoglobulin light-chain recombination by the transcription factor IRF-4 and the attenuation of interleukin-7 signaling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49859
Expression analysis from Runx2-deficient pDCs from mouse
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Plasmacytoid dendritic cells (pDCs) rapidly produce type I interferon (IFN-I) in response to viruses and are essential for antiviral immune responses. Although related to classical dendritic cells (cDCs) in their development and expression profile, pDCs possess many distinct features. Unlike cDCs, pDCs develop in the bone marrow (BM) and emerge into peripheral lymphoid organs and tissues as fully differentiated cells. We now report that pDCs specifically express Runx2, a Runt family transcription factor that is essential for bone development. Runx2-deficient murine pDCs developed normally in the BM but were greatly reduced in the periphery. The defect was cell-intrinsic and was associated with the retention of mature Ly49Q+ pDCs in the BM. Runx2 was required for the expression of several pDC-enriched genes including chemokine receptors Ccr2 and Ccr5. Mature pDCs expressed high levels of Ccr5 at the surface, and Ccr5-deficient pDCs in a competitive setting were reduced in the periphery relative to the BM. Thus, Runx2 is required for the emergence of mature BM pDCs into the periphery, in a process that is partially dependent on Ccr5. These results establish Runx2 as a lineage-specific regulator of immune system development.

Publication Title

Transcription factor Runx2 controls the development and migration of plasmacytoid dendritic cells.

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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