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accession-icon GSE80814
IL-2 therapy restores regulatory T cell dysfunction induced by calcineurin inhibitors
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

CNIs drastically modify the Treg specific transcriptional program in vivo in an IL-2 dependent manner

Publication Title

IL-2 therapy restores regulatory T-cell dysfunction induced by calcineurin inhibitors.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP133227
RNA Seq data: A375, A375R, A375DR vorinostat treated, and biopy samples from patients pre- and post- treated with Vorinostat
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

BRAF(V600E) mutant melanomas treated with inhibitors of the BRAF and MEK kinases almost invariably develop resistance, which is frequently caused by reactivation of the Mitogen Activated Protein Kinase (MAPK) pathway. To identify novel treatment options for such patients, we searched for acquired vulnerabilities of MAPK inhibitor-resistant melanomas. We find that resistance to BRAF+MEK inhibitors is associated with increased levels of reactive oxygen species (ROS). Subsequent treatment with the histone deacetylase inhibitor (HDACi) vorinostat represses SLC7A11 that leads to a lethal increase in the already elevated levels of ROS in drug-resistant cells, thereby causing selective apoptotic death of only the drug resistant tumor cells. Consistently, treatment of BRAF inhibitor-resistant melanoma with HDACi in mice results in a dramatic tumor regression. In a study in patients with advanced BRAF+MEK inhibitor resistant melanoma, we find that HDACi can selectively ablate drug-resistant tumor cells, providing clinical proof of concept for the novel therapy identified here. Overall design: one replicate of RNA Seq data A375, A375R, A375DR vorinostat treated and patient samples pre- post- vorinostat treatment

Publication Title

An Acquired Vulnerability of Drug-Resistant Melanoma with Therapeutic Potential.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line, Treatment, Subject

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accession-icon SRP106077
YY1 haploinsufficiency causes an intellectual disability syndrome featuring transcriptional and chromatin dysfunction [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 207 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Yin and yang 1 (YY1) is a well-known zinc-finger transcription factor with crucial roles in normal development and malignancy. YY1 acts both as a repressor and an activator of gene expression. We have identified 23 individuals with de novo mutations or deletions of YY1 and phenotypic features that define a syndrome of cognitive impairment, behavioral alterations, intrauterine growth retardation, feeding problems, and various congenital malformations. Our combined clinical and molecular data define the 'YY1 syndrome' as a haploinsufficiency syndrome. Through immunoprecipitation of YY1-bound chromatin from person-derived cells, using antibodies recognizing both ends of the protein, we show that YY1 deletions and missense mutations lead to a global loss of YY1 binding, with a preferential retention at high-occupancy sites. Finally, we uncover a widespread loss of H3K27 acetylation in particular on the YY1-bound enhancers, underscoring a crucial role for YY1 in enhancer regulation. Collectively, these results define a clinical syndrome caused by haploinsufficiency of YY1 through dysregulation of key transcriptional regulators. Overall design: Individuals with mutations or deletion in YY1 were identified among patients with idiopathic intellectual disability. LCLs were established from 4 of these patients (1 deletion, 2 missense mutations, and 1 non-sense mutation undergoing non-sense-mediated decay) as well as from unrelated controls, and their transcriptome were compared.

Publication Title

YY1 Haploinsufficiency Causes an Intellectual Disability Syndrome Featuring Transcriptional and Chromatin Dysfunction.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE43802
Characterization of Snail-associated small RNAs in colon cancer cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP018284
Identification of differentially expressed small RNAs of colon cancer stem cells.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

Colorectal carcinoma (CRC) is one of the most common cancers worldwide. Re-evaluating our current knowledge on CRC and developing novel therapeutic strategies is still crucial. Accumulating evidence suggests that cancer cells possess characters reminiscent of those of normal stem cells. Unveiling small RNAs responsible for cell stemness and chemoradioresistance should eventually lead to the development of novel therapeutic approaches. Overall design: Expression profiles of parental CRC cells and cancer spheres expanded under stem cell medium cultivation were generated for identifying key regulators.

Publication Title

MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE37596
Role of miR-146a in colon cancer cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

miRNAs exert various biological functions by targeting different cellular targets. Studying miR-146a functions in colon cancer cells helps to understand colorectal cancer (CRC) malignancy and progression.

Publication Title

MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

Sample Metadata Fields

Cell line

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accession-icon SRP135904
CRISPR-Cas9-based editing of histone H3 arginine 17 reveals its methylation-dependent regulation of Yap signaling and early mouse embryo development (RNA-seq data set)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We use rAPOBEC-XTEN-Cas9n-UGI (BE3) to introduce a point mutation (R17H) into 8 loci of Hist1H3 by a single sgRNA and a pre-stop codon into Carm1 in early mouse embryo, and both strategies resulted in developmental defects in pre-implantation embryos and fetal stages with smaller or developmental-delayed embryos. Transcriptomic analysis revealed that Yap1 and cell cycle signaling pathways were dysregulated in Carm1 pre-stop and H3R17H embryos, and Yap1 overexpression could rescue the developmental defects. Our results establish the direct regulatory relationship between Carm1-mediated site-specific histone modifications and mouse embryo development, and we also demonstrate that Hippo-Yap1 acts downstream of Carm1-mediated H3R17me2a to regulate the embryonic development and size determination. Overall design: Examination of RNA expression profiles of E4.5 WT/H3R17H/Carm1-/- mouse embryos by deep sequencing.

Publication Title

Base-Editing-Mediated R17H Substitution in Histone H3 Reveals Methylation-Dependent Regulation of Yap Signaling and Early Mouse Embryo Development.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE83912
Chip data of OsMYB30 overexpression and mutant plants under cold stress
  • organism-icon Oryza sativa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

It is important to reveal the regulatory mechanism of OsMYB30 gene which participated in cold response.

Publication Title

The OsMYB30 Transcription Factor Suppresses Cold Tolerance by Interacting with a JAZ Protein and Suppressing β-Amylase Expression.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP011546
Tracing pluripotency of human early embryos and embryonic stem cells by single cell RNA-seq
  • organism-icon Homo sapiens
  • sample-icon 116 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Find the casual relationship between gene expression network and cellular phenotype at single cell resolution. We collected donated human pre-implatation embryos, and the embryonic stem cells derived from them, isolate individual cells, prepared single cell cDNAs, and sequenced them by HiSeq2000. Then we analyzed the expression of known RefSeq genes. Overall design: We get transcriptome of 124 individual cells from human pre-implantation embryos and human embryonic stem cells by applying single cell RNA-seq technique we recently developed[1][2][3][4]. We did in-depth bioinformatic analysis to these data and found very dynamic expression of protein-coding genes. [1] Tang, F. et al. (2010a) Tracing the Derivation of Embryonic Stem Cells from the Inner Cell Mass by Single-Cell RNA-Seq Analysis. Cell Stem Cell 6, 468-478. [2] Tang, F. et al. (2010b) RNA-Seq analysis to capture the transcriptome landscape of a single cell. Nat Protocols 5, 516-535. [3] Tang, F. et al. (2009) mRNA-Seq whole-transcriptome analysis of a single cell. Nat Meth 6, 377-382. [4] Tang, F. et al. (2011) Development and applications of single-cell transcriptome analysis. Nat Meth 8, S6-S11.

Publication Title

Single-cell RNA-Seq profiling of human preimplantation embryos and embryonic stem cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP026144
Characterization of miRNomes in acute and chronic myeloid leukemia cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

An in-depth analysis of miRNomes in 3 human myeloid leukemia cell lines was carried out to comprehensively identify miRNAs that distinguish acute and chronic myeloid leukemias and relate to myeloid cell differentiation. Overall design: Characterization the miRNomes in 3 myeloid leukemia cell lines.

Publication Title

Characterization of miRNomes in acute and chronic myeloid leukemia cell lines.

Sample Metadata Fields

Specimen part, Disease, Cell line, 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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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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