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accession-icon GSE34378
Aging Experiment
  • organism-icon Mus musculus
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Lifelong murine gene expression profiles in relation to chronological and biological aging in multiple organs

Publication Title

Life spanning murine gene expression profiles in relation to chronological and pathological aging in multiple organs.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE31958
Expression data from primary mouse embryonic fibroblasts from wild-type and Cry double-knockout embryos
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

By gating cell cycle progression to specific times of the day, the intracellular circadian clock is thought to reduce the exposure of replicating cells to potentially hazardous environmental and endogenous genotoxic compounds. Although core clock gene defects that eradicate circadian rhythmicity can cause an altered in vivo genotoxic stress response and aberrant proliferation rate, it remains to be determined to what extent these cell-cycle-related phenotypes are due to a cell-autonomous lack of circadian oscillations. We investigated the DNA damage sensitivity and proliferative capacity of cultured primary Cry1-/-|Cry2-/- fibroblasts. Contrasting previous in vivo studies, we show that the absence of CRY proteins does not affect the cell-autonomous DNA damage response upon exposure of primary cells in vitro to genotoxic agents, but causes cells to proliferate faster. By comparing primary wild type, Cry1-/-|Cry2-/-, Cry1+/-|Cry2-/- and Cry1-/-|Cry2+/- fibroblasts, we provide evidence that CRY proteins influence cell cycle progression in a cell-autonomous, but circadian clock-independent manner and that the accelerated cell cycle progression of Cry-deficient cells is caused by global dysregulation of Bmal1-dependent gene expression. These results suggest that the inconsistency between in vivo and in vitro observations might be attributed to systemic circadian control rather than a direct cell-autonomous control.

Publication Title

Mammalian cryptochromes impinge on cell cycle progression in a circadian clock-independent manner.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE65780
Extensive translational regulation during seed germination revealed by translational profiling
  • organism-icon Arabidopsis thaliana
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.1 ST Array (aragene11st)

Description

We analysed the translatome and transcriptome of Arabidopsis thaliana Col-0 WT at five distinct physiological states during seed germination.

Publication Title

Extensive translational regulation during seed germination revealed by polysomal profiling.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE10609
the recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-ALL
  • organism-icon Homo sapiens
  • sample-icon 92 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner possibly delineating specific T-ALL subgroups. One subgroup, including MLL-rearranged, CALM-AF10 or inv(7)(p15q34) cases, is characterized by elevated expression of HOXA genes. Using a gene expression based clustering analysis of 67 T-ALL cases with recurrent molecular genetic abnormalities and 25 samples lacking apparent aberrations, we identified 5 new cases with elevated HOXA levels. Using array-CGH, a cryptic and recurrent deletion, del(9)(q34.11q34.13), was exclusively identified in 3 of these 5 cases. This deletion results in a conserved SET-NUP214 fusion product, that was also identified in the T-ALL cell line LOUCY. SET-NUP214 binds in the promoter regions of specific HOXA genes, where it may interact with CRM1 and DOT1L leading to the transcriptional activation of HOXA genes. Targeted inhibition of SET-NUP214 by siRNA abolished expression of HOXA genes, inhibited proliferation and induced differentiation in LOUCY but not in other T-ALL lines. We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

Publication Title

The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE37396
The histone methyltransferase MLL3 regulates genome-scale circadian transcription
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone methyltransferase MLL3 contributes to genome-scale circadian transcription.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE37387
Transcript levels in mouse liver
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Total RNA was isolated from liver samples of C57/BL6 mice over a circadian time course, 3 biological replicate samples per time point were collected and processed individually. RNA from each individual biological replicate sample was extracted using RNeasy mini kit (Qiagen Cat# 74106) and hybridized on an Affymetrix mouse Gene ST1.0 microarray.

Publication Title

Histone methyltransferase MLL3 contributes to genome-scale circadian transcription.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE9385
Identification of differentially regulated splice variants and novel exons in glial brain tumors using exon arrays
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aberrant splice variants are involved in the initiation and/or progression of glial brain tumors. We therefore set out to identify splice variants that are differentially expressed between histological subgroups of gliomas. Splice variants were identified using a novel platform that profiles the expression of virtually all known and predicted exons present in the human genome. Exon-level expression profiling was performed on 26 glioblastomas, 22 oligodendrogliomas and 6 control brain samples. Our results demonstrate that Human Exon arrays can identify subgroups of gliomas based on their histological appearance and genetic aberrations. We next used our expression data to identify differentially expressed splice variants. In two independent approaches, we identified 49 and up to 459 exons that are differentially spliced between glioblastomas and oligodendrogliomas a subset of which (47% and 33%) were confirmed by RT-PCR. In addition, exon-level expression profiling also identified >700 novel exons. Expression of ~67% of these candidate novel exons was confirmed by RT-PCR. Our results indicate that exon-level expression profiling can be used to molecularly classify brain tumor subgroups, can identify differentially regulated splice variants and can identify novel exons. The splice variants identified by exon-level expression profiling may help to detect the genetic changes that cause or maintain gliomas and may serve as novel treatment targets.

Publication Title

Identification of differentially regulated splice variants and novel exons in glial brain tumors using exon expression arrays.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13425
Expression data from ALL patients included in the set used to construct a classification signature (COALL cohort)
  • organism-icon Homo sapiens
  • sample-icon 190 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Childhood acute lymphoblastic leukemia (ALL) comprises a large group of genetic subtypes with a favorable prognosis characterized by a TEL-AML1-fusion, hyperdiploidy (>50 chromosomes) or E2A-PBX1 fusion and a smaller group with unfavorable outcome characterized by either a BCR-ABL-fusion, MLL-rearrangement or T-ALL.

Publication Title

A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13351
Expression data from ALL samples for patients included in the Dutch Childhood Oncology Group
  • organism-icon Homo sapiens
  • sample-icon 103 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Childhood acute lymphoblastic leukemia (ALL) comprises a large group of genetic subtypes with a favorable prognosis characterized by a TEL-AML1-fusion, hyperdiploidy (>50 chromosomes) or E2A-PBX1 fusion and a smaller group with unfavorable outcome characterized by either a BCR-ABL-fusion, MLL-rearrangement or T-ALL.

Publication Title

A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP013767
Transcriptome analysis of Drosophila neural stem cells reveals a transcriptional network for self-renewal.
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Illumina HiSeq 2000

Description

Drosophila neuroblasts have emerged as a model for stem cell biology that is ideal for genetic analysis but is limited by the lack of cell-type specific gene expression data. Here, we describe a methodology to isolate large numbers of pure neuroblasts and differentiating neurons that retain both cell cycle and lineage characteristics. We determine transcriptional profiles by mRNA sequencing and identify 28 predicted neuroblast specific transcription factors, which can be arranged in a network containing hubs for Notch signaling, growth control and chromatin regulation. Overexpression and RNAi for these factors identify Klumpfuss as a regulator of self-renewal. We show that loss of Klu function causes premature differentiation while overexpression results in the formation of transplantable brain tumors. Our data represent a valuable resource for Drosophila developmental neurobiology and we describes methodology that can be applied to other invertebrate stem cell lineages as well. Overall design: comparison of transcriptomes of Drosophila melanogaster larval neuroblasts and their differentiated daughter cells (neurons)

Publication Title

FACS purification and transcriptome analysis of drosophila neural stem cells reveals a role for Klumpfuss in self-renewal.

Sample Metadata Fields

Specimen part, 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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