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accession-icon GSE37476
Time course of gene expression changes after muscle contraction in spinal cord injured rats
  • organism-icon Rattus norvegicus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Purpose: The goal of this study was to determine the gene expression changes that occur over 7 days in parralyzed muscle in response to isometric contraction elicited by electrical stimulation initiated 4 months after spinal cord injury and to compare such changes to those observed in a normal muscle subjected to overload.

Publication Title

Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE52952
miRNAs trigger widespread epigenetically-activated siRNAs from transposons in Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE52067
miRNAs trigger widespread epigenetically-activated siRNAs from transposons inArabidopsis [Affymetrix]
  • organism-icon Arabidopsis thaliana
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Utilizing Affymetrix ATH1 microarrays to analyze transposon expression in DNA methylation mutants, and RNAi mutants, compared to wildtype.

Publication Title

miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE30301
Skeletal Muscle Contraction Reduces Effects of Unloading on Bone Independently from the Central Nervous System: Studies Using Functional Electrical Stimulation after Spinal Cord Transection
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Spinal cord injury (SCI) causes severe bone loss and disrupts connections between higher centers in the central nervous system (CNS) and bone. Muscle contraction elicited by functional electrical stimulation (FES) partially protects against loss of bone but cellular and molecular events by which this occurs are unknown. Here, using a rat model, we characterized effects of 7 days of contraction-induced loading of tibia and fibula due to FES when begun 16 weeks after SCI. SCI reduced tibial and femoral BMD by 12-17% and promoted bone resorption, as indicated by increased serum CTX; SCI-related changes in CTX were reversed by FES. In cultures of bone marrow cell-derived cells, SCI increased the number of osteoclasts and mRNA levels of the several osteoclast differentiation markers; these changes were significantly reversed by FES. The number of osteoblasts was also reduced by SCI as was the ratio of OPG/RANKL mRNAs therein; the unfavorable change in OPG/RANKL ratio was partially reversed by FES. cDNA microarray analysis revealed that alterations in genes involved in signaling through Wnt, FSH/LH, PTH and calcineurin/NFAT pathways may be linked to the favorable action of FES on SCI-induced bone resorption. In particular, SCI increased levels of the Wnt inhibitors DKK1, sFRP2 and SOST in osteoblasts, These effects were completely or partially reversed by FES. Our results demonstrate an anti-bone resorptive activity of acute FES in bone loss after SCI and suggest potential underlying mechanisms, among them involving increased Wnt signaling to cause more favorable ratios of OPG and RANKL for the inhibition of osteoclastogenesis. The present study indicates that the effects of bone reloading on SCI- related bone remodeling occurred independently of the effects of higher CNS centers on bone.

Publication Title

The central nervous system (CNS)-independent anti-bone-resorptive activity of muscle contraction and the underlying molecular and cellular signatures.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE56352
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.

Publication Title

Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE45725
Internal validation cohort of breast cancers for development of ClinicoMolecular Triad Classification
  • organism-icon Homo sapiens
  • sample-icon 340 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

In our early study (PMID: 21939527), we have created a ClinicoMolecular Triad Classification (CMTC) to improve prediction and prognostication of breast cancer by using a training cohort contained 161 breast cancer patients (2003 to 2008). Here, a supplemental internal validation cohort contained 340 breast cancer patients was collected (2008 to 2010) for development of the CMTC.

Publication Title

Validation of the prognostic gene portfolio, ClinicoMolecular Triad Classification, using an independent prospective breast cancer cohort and external patient populations.

Sample Metadata Fields

Age, Disease stage

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accession-icon GSE63165
The epigenetic modifier EZH2 controls melanoma growth and metastasis through silencing of distinct tumour suppressors
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Increased activity of the epigenetic modifier EZH2 has been associated with different cancers. However, evidence for a functional role of EZH2 in tumourigenesis in vivo remains poor, in particular in metastasising solid cancers. Here we reveal central roles of EZH2 in promoting growth and metastasis of cutaneous melanoma. In a melanoma mouse model, conditional Ezh2 ablation as much as treatment with the preclinical Ezh2 inhibitor GSK503 stabilises the disease through inhibition of growth and virtually abolishes metastases formation without affecting normal melanocyte biology. Comparably, in human melanoma cells, EZH2 inactivation impairs proliferation and invasiveness, accompanied by re-expression of tumour suppressors connected to increased patient survival. These EZH2 target genes suppress melanoma growth and prevent EMT / metastasis in vivo revealing the dual function of EZH2 in promoting tumour progression. Thus, EZH2-mediated epigenetic repression is highly relevant especially during advanced melanomagenesis, which makes EZH2 a promising target for novel melanoma therapies.

Publication Title

The epigenetic modifier EZH2 controls melanoma growth and metastasis through silencing of distinct tumour suppressors.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE56954
A687V EZH2 is a driver of histone H3 lysine 27 (H3K27) hyper-trimethylation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression changes were analyzed in 2 acute lymphoblastic leukemia cell lines treated with the GSK126 EZH2 inhibitor using Affymetrix Human Genome U133 Plus 2.0 arrays.

Publication Title

A687V EZH2 is a driver of histone H3 lysine 27 (H3K27) hypertrimethylation.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon SRP008118
Transcriptome-Wide Binding Sites for Components of the Saccharomyces cerevisiae Non-poly(A) termination Pathway: Nrd1, Nab3 and Sen1
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We report here the transcriptome-wide distribution of yeast Rpb2, Sen1, Nrd1 and Nab3 binding sites. These data sets provide highresolution definition of non-poly(A) terminators, identify novel genes regulated by attenuation of nascent transcripts close to the promoter, and demonstrate the widespread occurrence of Nrd1-bound 3'-antisense transcripts on genes that are poorly expressed. In addition, we show that Sen1 does not cross-link to many expected ncRNAs but surprisingly binds to pre-mRNA transcripts suggesting a role in 3' end formation and/or termination. Overall design: Six samples by adaptation of PAR-ClIP procedure

Publication Title

Yeast Nrd1, Nab3, and Sen1 transcriptome-wide binding maps suggest multiple roles in post-transcriptional RNA processing.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE3166
Influence of cyclical mechanical strain on global gene expression in human lamina cribrosa cells in vitro
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The mechanical effect of raised intraocular pressure is a recognised stimulus for optic neuropathy in primary open angle glaucoma (POAG). Characteristic extra-cellular matrix (ECM) remodelling accompanies axonal damage in the lamina cribrosa (LC) of the optic nerve head in POAG. Glial cells in the lamina cribrosa may play a role in this process but the precise cellular responses to mechanical forces in this region are unknown. The authors examined global gene expression profiles in lamina cribrosa cells exposed to cyclical mechanical stretch, with an emphasis on ECM genes.

Publication Title

Influence of cyclical mechanical strain on extracellular matrix gene expression in human lamina cribrosa cells in vitro.

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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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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