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accession-icon GSE33442
The target genes of EGFR activity in glioma cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array.

Publication Title

Guanylate binding protein 1 is a novel effector of EGFR-driven invasion in glioblastoma.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE45935
Exon level gene expression profile of the prefrontal cortex region of Df(16)A+/- mice, a mouse model of 22q11.2 microdeletion syndrome
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex between mutant and wild type animals at exon level. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. Df(16)A+/- mice line is a model of human 22q11 microdeletion syndrome.

Publication Title

The pattern of cortical dysfunction in a mouse model of a schizophrenia-related microdeletion.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP055677
RNA-seq analysis of add-back rescued TALEN-mediated LATS2 knockout HeLa-S3 cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Chromatin modifying activities for construction of appropriate epigenetic landscapes by polycomb repressive complex 2 (PRC2) play an essential role in development and tumorigenesis. However, the spatiotemporal mechanisms by which PRC2 achieves diverse epigenomes for specific tissue or cellular contexts remain poorly understood. Here, we discovered that LATS2 knockout causes dysregulation of PRC2 and subsequent transcriptome changes for differentiation in both mouse and human cells. LATS2 depletion dependent dysregulation of PRC2 also effects H3K4me3 and forms negative feedback loop for maintenance of PRC2. Further analyses reveal that LATS2 on chromatin binds to EZH2 and LATS2 has ability to phosphorylate PRC2 in vitro. These LATS2 dependent H3K27me3 targets are highly induced during neurogenesis, and statistical analysis of glioblastoma multiforme reveals that LATS2-high cases show more dedifferentiated transcriptome and poor prognosis with silencing of H3K27me3 targets. These observations suggest that LATS2-mediated epigenome coordination is pivotal for development and disease, including cancer. Overall design: mRNA of LATS2 KO HeLa-S3 cells rescued by empty vector, wild-type LATS2 or kinase-dead LATS2 were subjected to deep sequencing profiling using Illumina HiSeq 2500

Publication Title

LATS2 Positively Regulates Polycomb Repressive Complex 2.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE90791
Expression data of neuroblastoma tissues, spheres and NGP cell line overexpressing CFC1
  • organism-icon Homo sapiens
  • sample-icon 4 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

CFC1 is a cancer stemness-regulating factor in neuroblastoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE19678
DACH1 expression in U87 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Loss or reduction in function of tumor suppressor genes contributes to tumorigenesis. We identified a novel homozygous deletion of DACH1 in gliomas.

Publication Title

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE42392
Expression analysis of cancer of unknown primary (CUP)
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Biopsies (lymph nodes, ascites or hydrothorax) from 60 patients with cancer of unknown primary origin were analyzed.

Publication Title

A microarray-based gene expression analysis to identify diagnostic biomarkers for unknown primary cancer.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP049674
Epigenomic Signatures of Neuronal Diversity in the Mammalian Brain
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

We developed an affinity purification approach to isolate tagged nuclei in mice (similar to INTACT; [Deal R.B. and Henikoff S. A simple method for gene expression and chromatin profiling of individual cell types within a tissue. Dev. Cell 18,1030-1040. (2010)]) and used it to characterize genome-wide patterns of transcription, DNA methylation, and chromatin accessibility in 3 major neuron classes of the neocortex (excitatory pyramidal neurons, parvalbumin (PV)-positive GABAergic interneurons, and vasoactive intestinal peptide (VIP)-positive GABAergic interneurons). By combining cell purification and integrative analysis, our findings relate the phenotypic and functional complexity of neocortical neurons to their underlying transcriptional and epigenetic diversity. Overall design: RNA-seq, MethylC-seq, ATAC-seq, and ChIP-seq for histone modifications using INTACT-purified nuclei from the mouse neocortex

Publication Title

Epigenomic Signatures of Neuronal Diversity in the Mammalian Brain.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41050
Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues
  • organism-icon Homo sapiens
  • sample-icon 14 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

Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE41049
Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues (Gene Expression data)
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

DNA methylation has been comprehensively profiled in normal and cancer cells, but the dynamics that form, maintain and reprogram differentially methylated regions remain enigmatic. We show that methylation patterns within populations of cells from individual somatic tissues are heterogeneous and polymorphic. Using in vitro evolution of immortalized fibroblasts for over 300 generations, we track the dynamics of polymorphic methylation at regions developing significant differential methylation on average. The data indicate that changes in population-averaged methylation occur through a stochastic process that generates a stream of local and uncorrelated methylation aberrations. Despite the stochastic nature of the process, nearly deterministic epigenetic remodeling emerges on average at loci that lose or gain resistance to methylation accumulation. Changes in the susceptibility to methylation accumulation are correlated with changes in histone modifications and CTCF occupancy. Characterizing epigenomic polymorphism within cell populations is therefore critical for understanding methylation dynamics in normal and cancer cells.

Publication Title

Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP012289
The post-apoptotic fate of RNAs identified through high-throughput sequencing of human hair
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina Genome Analyzer II

Description

The hair of all mammals consists of terminally differentiated cells that undergo a specialized form of apoptosis called cornification. While DNA is destroyed during cornification, the extent to which RNA is lost is unknown. Here we find that multiple types of RNA are incompletely degraded after hair shaft formation in both mouse and human. Notably, mRNAs and short regulatory microRNAs (miRNAs) are stable in the hair as far as 10 cm from the scalp. To better characterize the post-apoptotic RNAs that escape degradation in the hair, we performed sequencing (RNA-seq) on RNA isolated from hair shafts pooled from several individuals. This hair shaft RNA library, which encompasses different hair types, genders, and populations, revealed 7,193 mRNAs, 449 miRNAs and thousands of unannotated transcripts that remain in the post-apoptotic hair. A comparison of the hair shaft RNA library to that of viable keratinocytes revealed surprisingly similar patterns of gene coverage and indicates that degradation of RNA is highly inefficient during apoptosis of hair lineages. The generation of a hair shaft RNA library could be used as months of accumulated transcriptional history useful for retrospective detection of disease, drug response and environmental exposure.

Publication Title

The post-apoptotic fate of RNAs identified through high-throughput sequencing of human hair.

Sample Metadata Fields

No sample metadata fields

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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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