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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

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accession-icon SRP051485
Pervasive transcription read-through promotes aberrant expression of oncogenes and RNA chimeras in renal carcinoma
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Aberrant expression of cancer genes and non-canonical RNA species is a hallmark of cancer. However, the mechanisms driving such atypical gene expression programs are incompletely understood. Here, our transcriptional profiling of a cohort of 50 primary clear cell renal cell carcinoma (ccRCC) samples from The Cancer Genome Atlas (TCGA) reveals that transcription read-through beyond the termination site is a source of transcriptome diversity in cancer cells. Amongst the genes most frequently mutated in ccRCC, we identified SETD2 inactivation as a potent enhancer of transcription read-through. We further show that invasion of neighbouring genes and generation of RNA chimeras are functional outcomes of transcription read-through. We identified the BCL2 oncogene as one of such invaded genes and detected a novel chimera, the CTSC-RAB38, in 20% of ccRCC samples. Collectively, our data highlight a novel link between transcription read-through and aberrant expression of oncogenes and chimeric transcripts that is prevalent in cancer. Overall design: RNA-seq of SETD2 mutant and wild-type ccRCC cell lines.

Publication Title

Pervasive transcription read-through promotes aberrant expression of oncogenes and RNA chimeras in renal carcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE45551
Prevention of Mouse AA with IL-15 pathway inhibitors
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Our goal was to identify gene expression patterns that correlated with prevention of autoimmune alopecia in C3H/HeJ mice following alopecic graft transplantation

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE45514
Treatment of established mouse AA with topical JAK inhibitors
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Our goal was to identify gene expression patterns that correlated with treatment of established autoimmune alopecia in C3H/HeJ mice following alopecic graft transplantation

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE45512
Human Alopecia Areata Skin Profiling
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our goal was to develop a transcriptomic description of affected alopecic scalp skin from patients with alopecia areata.

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part

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accession-icon GSE58573
First ruxolitinib treatment of human alopecia areata patients
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Two patients with alopecia areata were treated with systemic ruxolitinib. Skin biopsies were taken before starting treatment and 12 weeks after starting treatment.

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part, Disease, Treatment

View Samples
accession-icon GSE45513
Mouse Spontaneous C3H/HeJ AA Skin
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Our goal was to develop a transcriptomic description of affected alopecic skin from aged C3H/HeJ mice. Affected skin from 3 mice was compared to skin from similarly aged but unaffected C3H/HeJ mice.

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE64932
Transcriptome study of colon epithelial cells in Reg3a-transgenic mice
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The human C-type lectin Reg3a (HIP/PAP) is an antimicrobial peptide that kills Gram-positive bacteria. Reg3a preserves gut microbiota homeostasis, reinforces intestinal barrier function and thereby helps to fight induced colitis in mice.

Publication Title

Enteric Delivery of Regenerating Family Member 3 alpha Alters the Intestinal Microbiota and Controls Inflammation in Mice With Colitis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE92861
Expression data from individual MEF2A isoform knockdown in neonatal rat ventricular myocytes (NRVMs)
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

Regulation of homeostasis and development of cardiac muscle tissues is controlled by a core set of transcription factors. The MEF2 family plays a critical role in these processes.

Publication Title

Antagonistic regulation of cell-cycle and differentiation gene programs in neonatal cardiomyocytes by homologous MEF2 transcription factors.

Sample Metadata Fields

Specimen part

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accession-icon GSE54500
Role of H3K79 methylation states in HOX gene expression and leukemogenesis
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.

Sample Metadata Fields

Specimen part, Disease

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)

fund-icon Fund the CCDL

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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