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accession-icon SRP092098
Analysis of genes differencially expressed depending on Myc expression
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal is to examine the transcriptome of ESCs with different Myc levels Overall design: In order to analyse the transcriptome, mESC population was sorted in 3 groups depending on Myc levels

Publication Title

Pluripotency Surveillance by Myc-Driven Competitive Elimination of Differentiating Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP110619
RNA-Seq analysis of iMOS T1-Myc ESC mosaic cultures
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

The goal of this study is to analyse the transcriptome of WT and Myc-overexpressing ESCs in iMOS T1-Myc mosaic cultures. Overall design: Homozygous iMOS T1-Myc ESC cultures (Claveria et al., 2013) were treated with 20µM 4-hydroxytamoxifen for 24 hours to generate a mosaic of cell populations containing two, one or no extra Myc and EYFP copies. 24 hours after tamoxifen removal, cells were sorted according to their EYFP expression levels and populations with two extra Myc and EYFP copies and with no extra Myc and EYFP copies were collected. Uninduced homozygous iMOS T1-Myc ESC cultures were also sorted and collected as a control. Three biological replicas were included for each condition.

Publication Title

Pluripotency Surveillance by Myc-Driven Competitive Elimination of Differentiating Cells.

Sample Metadata Fields

Subject

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accession-icon GSE94341
Inhibition of the kinesin spindle protein enhances the activity of pomalidomide and dexamethasone in multiple myeloma
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE94336
Inhibition of the kinesin spindle protein enhances the activity of pomalidomide and dexamethasone in multiple myeloma [In Vivo]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Kinesin spindle protein (KSP) inhibition is known to be an effective therapeutic approach in several malignancies. Filanesib (Arry-520), a KSP inhibitor, has demonstrated activity in heavily pretreated multiple myeloma (MM) patients. The aim of this work was to investigate the activity of filanesib in combination with an IMiDs plus dexamethasone backbone, and the mechanisms underlying the potential synergistic effect. Results: Filanesib showed in vitro and in vivo synergy with all IMiDs plus dexamethasone treatment, particularly with the pomalidomide combination (PDF). Importantly, the in vivo synergy observed in this combination was more evident in large, highly proliferative tumors, and it was shown to be mediated by impairment of mitosis transcriptional control, an increase in monopolar spindles, cell cycle arrest and the induction of apoptosis in cells in proliferative phases. In addition, PDF increased the activation of the proapoptotic protein Bax, which has been previously associated with sensitivity to filanesib, and could potentially be used as a predictive biomarker of response to this combination. Conclusions: Our results provide preclinical evidence for the potential benefit of the combination of filanesib with pomalidomide and dexamethasone and es-tablished the basis for a recently activated trial being conducted by the Spanish MM group investigating this combination in relapsed MM patients.

Publication Title

The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE94334
Inhibition of the kinesin spindle protein enhances the activity of pomalidomide and dexamethasone in multiple myeloma [In Vitro]
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Kinesin spindle protein (KSP) inhibition is known to be an effective therapeutic approach in several malignancies. Filanesib (Arry-520), a KSP inhibitor, has demonstrated activity in heavily pretreated multiple myeloma (MM) patients. The aim of this work was to investigate the activity of filanesib in combination with an IMiDs plus dexamethasone backbone, and the mechanisms underlying the potential synergistic effect. Results: Filanesib showed in vitro and in vivo synergy with all IMiDs plus dexamethasone treatment, particularly with the pomalidomide combination (PDF). Importantly, the in vivo synergy observed in this combination was more evident in large, highly proliferative tumors, and it was shown to be mediated by impairment of mitosis transcriptional control, an increase in monopolar spindles, cell cycle arrest and the induction of apoptosis in cells in proliferative phases. In addition, PDF increased the activation of the proapoptotic protein Bax, which has been previously associated with sensitivity to filanesib, and could potentially be used as a predictive biomarker of response to this combination. Conclusions: Our results provide preclinical evidence for the potential benefit of the combination of filanesib with pomalidomide and dexamethasone and es-tablished the basis for a recently activated trial being conducted by the Spanish MM group investigating this combination in relapsed MM patients.

Publication Title

The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE7441
Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Amyotrophic lateral sclerosis (ALS) is caused by the progressive degeneration of motor neurons. Mutations in the Cu/Zn superoxide dismutase (SOD1) are found in about 20% of patients with familial ALS. Mutant SOD1 causes motor neuron death through an acquired toxic property. Although, molecular mechanism underlying this toxic gain-of-function remains unknown, evidence support the role of mutant SOD1 expression in non-neuronal cells in shaping motor neuron degeneration. We have previously found that in contrast to non-transgenic, SOD1G93A-expressing astrocytes induced apoptosis of co-cultured motor neurons. This prompted us to investigate whether the effect on motor neuron survival was related to a change in the gene expression profile. Through high-density oligonucletide microarrays we found changes in the expression of genes involved in transcription, signaling, cell proliferation, extracellular matrix construction, response to stress and steroid and lipid metabolism. Decorin, a small multifunctional proteoglycan, was the most up-regulated gene. Down-regulated genes included the insulin-like growth factor-1 receptor and the RNA binding protein ROD1. We also analyzed the expression of selected genes in purified motor neurons expressing SOD1G93A and in spinal cord of asymptomatic and early symptomatic ALS-rodent model.

Publication Title

Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP096672
Regulation of mRNA translation and subcellular location controls protein synthesis of key modulators of the DNA damage response during B cell activation [PolyRiboSeq]
  • organism-icon Mus musculus
  • sample-icon 157 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Post-transcriptional regulation of cellular mRNA is essential for protein synthesis. Here we describe the importance of mRNA translational repression and mRNA subcellular location for protein expression during B lymphocyte activation and the DNA damage response. Cytoplasmic RNA granules are formed upon cell activation with mitogens, including stress granules that contain the RNA binding protein Tia1. Tia1 binds to a subset of transcripts involved in cell stress, including p53 mRNA, and controls translational silencing and RNA granule localization. DNA damage promotes mRNA relocation and translation in part due to dissociation of Tia1 from its mRNA targets. Upon DNA damage, p53 mRNA is released from stress granules and associates with polyribosomes to increase protein synthesis. Global analysis of cellular mRNA abundance and translation indicates that this is an extended ATM-dependent mechanism to increase protein expression of key modulators of the DNA damage response. Overall design: Splenic B cells from C57BL/6Babr mice were isolated and activated with LPS for 48 hours prior induction or not of DNA damage with etoposide. After 4 hours, cells were treated with cycloheximide (100 microgrames per ml) for 3 minutes. Then, cytoplasmic extracts were collected. Polysome fractionation in sucrose gradients (10-50% sucrose) was performed for isolation of mRNA associated to monosomes (fractions 4 to 7), light polysomes (fractions 8 to 10) or heavy polysomes (fractions 11 to 16). The ATM kinase inhibitor KU55933 was added 1 hour prior induction of DNA damage with etoposide.

Publication Title

Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE98595
Cabergoline-treated lutein granulosa cells from polycystic ovarian syndrome (PCOS) patients exhibit higher transcriptomic response than cabergoline-treated controls
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This study assessed the transcriptomic profiles of lutein granulosa cells (LGCs) from women with and without PCOS using Affymetrix microarray chips to provide novel information about the molecular changes that occur in these cells when they are treated with a D2-ag (Cb2) and to assess the signal transduction pathways regulated by this treatment.

Publication Title

Dysregulated genes and their functional pathways in luteinized granulosa cells from PCOS patients after cabergoline treatment.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE45044
Age-mediated transcriptomic changes in adult mouse brain ventral tegmental area
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Substantia nigra pars compacta (SNpc) is highly sensitive to normal aging and selectively degenerates in Parkinson's disease. However, ventral tegmental area (VTA), a region adjacent to SNpc, is less affected in PD. Until now, molecular mechanisms behind VTA aging have not been fully investigated using high throughput techniques.

Publication Title

Age-mediated transcriptomic changes in adult mouse substantia nigra.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE45043
Age-mediated transcriptomic changes in adult mouse substantia nigra
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Substantia nigra pars compacta (SNpc) is highly sensitive to normal aging and selectively degenerates in Parkinson's disease. Until now, molecular mechanisms behind SNpc aging have not been fully investigated using high throughput techniques.

Publication Title

Age-mediated transcriptomic changes in adult mouse substantia nigra.

Sample Metadata Fields

Specimen part

View Samples

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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