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accession-icon GSE44649
Expression data from wild-type and microRNA-155 (miR-155) deficient CD8 T cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

MicroRNA-155 (miR-155) is upregulated in primary effector CD8 T cells but is expressed at low amounts in nave cells. Anti-viral CD8 T cell responses and viral clearance were impaired in miR-155 deficient (bic-/-) mice, and this defect was intrinsic to CD8 T cells, as adoptively transferred bic-/- CD8 T cells generated greatly reduced primary and memory responses during infection. To understand the mechanism by which miR-155 regulates CD8 T cell activation, we analyzed the gene expression profiles of naive and in vitro activated wild-type and bic-/- CD8 T cells.

Publication Title

The microRNA miR-155 controls CD8(+) T cell responses by regulating interferon signaling.

Sample Metadata Fields

Specimen part

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accession-icon GSE65503
Radiation and Dual Checkpoint Blockade Activates Non-Redundant Mechanisms in Cancer
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Response to immune checkpoint inhibitors may be improved through combinations with each other and other therapies, raising questions about non-redundancy and resistance. We report results from parallel studies of melanoma patients and mice treated with anti-CTLA4 and radiation (RT). Although combined treatment improved responses, resistance was common. Computational analyses of immune and transcriptomic profiles (provided here) revealed that resistance in mice was due to upregulation of tumor PD-L1 that drives T cell exhaustion. Accordingly, optimal response requires RT, anti-CTLA4, and anti-PD-L1. Anti-CTLA4 inhibits Tregs, RT diversifies and shapes the TCR repertoire, and anti-PD-L1 reinvigorates exhausted T cells. Together, all three therapies promote the expansion of clonotypes with distinct TCR traits. Similar to mice, patients with melanoma showing high PD-L1 did not respond to RT + anti-CTLA4, demonstrated persistent T cell exhaustion, and rapidly progressed. Thus, the combination of RT, anti-CTLA4, and anti-PD-L1 promotes response through distinct mechanisms.

Publication Title

Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20907
Intrinsic response of thoracic propriospinal neurons to axotomy
  • organism-icon Rattus norvegicus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Analysis of expression changes in prelabeled laser-microdissected thoracic propriospinal neurons at different times after low-thoracic spinal cord transection in adult rats.

Publication Title

Intrinsic response of thoracic propriospinal neurons to axotomy.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE27362
Expression data from parthenogenetic and WT iPS samples and their parental fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Three parthenogenetic induced pluripotent stem cell (PgHiPSCs) lines were generated from each of the ovarian teratoma cell lines (two distinct individuals). Two normal iPS cell lines were generated from normal fibroblasts. Three biological replicates of normal embryonic stem cells (H9, HESCs) were perfomed.

Publication Title

Global analysis of parental imprinting in human parthenogenetic induced pluripotent stem cells.

Sample Metadata Fields

Sex, Cell line

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accession-icon GSE56136
The noncoding RNA IPW regulates the imprinted DLK1-DIO3 locus in an induced pluripotent stem cell model of Prader-Willi syndrome
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Parental imprinting is a form of epigenetic regulation that results in parent-of-origin differential gene expression. To study Prader-Willi syndrome (PWS), a developmental imprinting disorder, we generated patient-derived induced pluripotent stem cells (iPSCs) harboring distinct deletions in the affected region on chromosome 15. Studying PWS-iPSCs and human parthenogenetic iPSCs unexpectedly revealed substantial upregulation of virtually all maternally expressed genes (MEGs) in the imprinted DLK1-DIO3 locus on chromosome 14. Subsequently, we identified IPW, a long noncoding RNA in the critical region of the PWS locus, as a regulator of the DLK1-DIO3 region, as its over-expression in PWS and parthenogenetic iPSCs results in downregulation of the MEGs in this locus. We further show that gene expression changes in the DLK1-DIO3 region coincide with chromatin modifications, rather than DNA methylation levels. Our results suggest that a subset of PWS phenotypes may arise from dysregulation of an imprinted locus distinct from the PWS region.

Publication Title

The noncoding RNA IPW regulates the imprinted DLK1-DIO3 locus in an induced pluripotent stem cell model of Prader-Willi syndrome.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP079189
Dysregulated synaptic gene expression and axonal neuropathology in a human iPSC-based model of familial Parkinson''s disease
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We generated de novo induced pluripotent stem cells (iPSCs) from two Parkinson’s Disease patients (PD) harboring the p.A53T mutation. iPSC-derived mutant neurons displayed disease-relevant phenotypes at basal conditions, including protein aggregation, compromised neuritic outgrowth and contorted axons with swollen varicosities containing aSyn and tau. We have performed RNA Sequencing (RNA-Seq) of neurons from PD patient and control samples. RNA sequencing has also been performed to neurons derived from HUES samples subjected to the same differentiation protocol as reference. Overall design: We have performed RNA Sequencing (RNA-Seq) in neurons PD and control samples (two clones from each individual), along with HUES-derived neurons.

Publication Title

Defective synaptic connectivity and axonal neuropathology in a human iPSC-based model of familial Parkinson's disease.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE6065
Murine host cell response to Aeromonas infection
  • organism-icon Mus musculus
  • sample-icon 268 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Aims: To assess the virulence of multiple Aeromonas spp. using two models, a neonatal mouse assay and a mouse intestinal cell culture.

Publication Title

Evaluating virulence of waterborne and clinical Aeromonas isolates using gene expression and mortality in neonatal mice followed by assessing cell culture's ability to predict virulence based on transcriptional response.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE32529
Mouse ischemic tolerance genomic analysis of the brain and blood.
  • organism-icon Mus musculus
  • sample-icon 224 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia.

Publication Title

Multiple preconditioning paradigms converge on interferon regulatory factor-dependent signaling to promote tolerance to ischemic brain injury.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE79598
Expression data from H9 human embryonic stem cells (hESCs) infected with either lentiviral non-silencing shRNA or shRUNX1, and differentiated to early mesendoderm
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

We used microarrays to detail the global program of gene expression during early hESC differentiation to mesendoderm using FBS, with and without RUNX1 depletion.

Publication Title

Transient RUNX1 Expression during Early Mesendodermal Differentiation of hESCs Promotes Epithelial to Mesenchymal Transition through TGFB2 Signaling.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE39857
The RALA pathway can maintain the proliferation of KRAS- and BRAF-mutated cancer cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis.

Publication Title

Effects of RAL signal transduction in KRAS- and BRAF-mutated cells and prognostic potential of the RAL signature in colorectal cancer.

Sample Metadata Fields

Specimen part, Cell line, 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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