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accession-icon GSE40610
Expression data from a Charcot-Marie-Tooth 1B neuropathy mouse model
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We have generated mouse models of real CMT1B mutations in the gene encoding for myelin protein zero (P0). One of these mutants, P0S63del is retained in the ER where it elicits an unfolded protein response (UPR). Genetic ablation of the UPR factor CHOP restores the motor capacity in S63del mice. We used microarray to decipher the molecular mechanism undelying the P0S63del neuropathy and the rescue in S63del/Chop null nerves.

Publication Title

Resetting translational homeostasis restores myelination in Charcot-Marie-Tooth disease type 1B mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE51925
Aged Mice are Unable to Mount an Effective Myeloid Response to Sepsis
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Old C57BL/6 mice cannot mount an effective innate immune response

Publication Title

Aged mice are unable to mount an effective myeloid response to sepsis.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE95759
Dust mite potently activates Th17/Th22 pathways and models multiple inflammatory skin conditions in humans
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

House dust mite/HDM atopy patch test/APT elicits positive reactions in the majority of atopic dermatitis/AD and healthy individuals. Experimental systems for new-onset/chronic AD are needed to support rapid therapeutic development, particularly since animal models representing AD pathology in humans are lacking. HDM APT historically simulated AD, but its suitability to model the emerging AD skin phenotype as Th2/Th22 polarized with Th1 and Th17 components is unknown. To assess whether HDM APT tissues reproduce acute or chronic AD, positive HDM APT (n=14) were compared with nonlesional, acute (<72hrs; n=10), and chronic phase AD biopsies (n=8), allergic contact reactions (to nickel [n=10] and fragrance [n=3]) using arrays.

Publication Title

Dust mite induces multiple polar T cell axes in human skin.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE70418
A Detailed Characterization of the Dysfunctional Immunity and Abnormal Myelopoiesis Induced by Severe Shock and Trauma in the Aged
  • organism-icon Mus musculus
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The polytrauma (PT) murine model has unique transcriptomic responses 2 hrs, 1 day and 3 days after injury. We determined with this clinically relevant model that the increased morbidity in the elderly is secondary to a failure of bone marrow progenitors, blood neutrophils, and bronchoalveolar lavage cells to initiate and complete an 'emergency myelopoietic' response, engendering myeloid cells that fail to clear secondary infection. In addition, the elderly appear unable to effectively resolve their inflammatory response to severe injury.

Publication Title

A Detailed Characterization of the Dysfunctional Immunity and Abnormal Myelopoiesis Induced by Severe Shock and Trauma in the Aged.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE37005
Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq
  • organism-icon Mus musculus, Homo sapiens, Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE36958
Gene expression profiles of WT and ime4-/- mutant yeast cells, under vegetative and meiosis-inducing conditions
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Inactivation of the yeast IME4 gene, the yeast homologue of METTL3, was shown to result in the loss of m6A in mRNA of mutant cells grown in sporulation medium. We attempted to characterize the effects of ime4 deletion on gene expression under vegetative and meiosis-inducing conditions. The results show that in vegetatively-growing ime4-/- cells there is an increased expression of the RME1 gene (repressor of meiosis) which prevents precocious entry into the meiotic program. Mutant yeast cells showed reduced expression levels of genes involved in ribosome biogenesis and gene expression processes. Surprisingly, despite the fact that a diploid strain was analyzed, there was also a striking change in the expression level of haploid-specific genes, suggesting that RNA methylation may be used to enforce the sexual identity of diploid cells, required for the implementation of the gametogenesis program. Consistently, when cells were induced to undergo meiosis, ime4-/- diploids failed to undergo the meiotic divisions. Among the genes showing reduced expression in the mutant were IME1 and IME2, the two known inducers of meiosis. Thus, the yeast IME4 gene plays an important role in the regulation of the developmental switch from vegetative cells into gametogenesis.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP012098
m6A mapping in human RNA (with treatments)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We developed a novel approach, m6A-seq, for high-resolution mapping of the transcriptome-wide m6A landscape, based on antibody-mediated capture followed by massively parallel sequencing. Overall design: Identification of m6A modified sequences in HepG2 cells. HepG2 cells were incubated with either IFNg (200ng/ml) or HGF/SF (10 ng/ml) over night. Stress effects were tested in HepG2 cells by either 30 minutes incubation at 43ºC (heat shock) or UV irradiation of 0.04 J/cm2 followed by 4 hours of recovery in normal growing conditions prior to harvesting using Trypsin.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP012096
METTL3 KD in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Overall design: Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP053794
RNA-Seq atopic dermatitis transcriptome profiling provides insights into novel disease mechanisms with potential therapeutic implications
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Purpose: provide evidence that RNA-seq can add information to transcriptome profiling already discovered by other technologies for atopic dermatitis Methods: mRNA profiles of 20 atopic dermatitis were analyzed to compare lesional and non-lesional skin, then transcriptomes found by reads were compared to Microarray and RT-PCR Results:RNA-seq provided complementary genes to AD transcriptome IL-36 and TREM-1 Conclusions: Our study represents the first analysis of lesional AD tissue by RNA-seq and comparison to microarray and RT-PCR Overall design: paired biopsies from lesional and non-lesional tissue of 20 patients sequenced by RNA-seq

Publication Title

RNA sequencing atopic dermatitis transcriptome profiling provides insights into novel disease mechanisms with potential therapeutic implications.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36098
Gene expression profile of human iPS cell-derived mesoangioblasts (HIDEMs)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mesoangioblasts are stem/progenitor cells derived from a subset of pericytes expressing alkaline phosphatase. They have been shown to ameliorate muscular dystrophies (currently incurable diseases) in different animal models and are now undergoing clinical experimentation for Duchenne muscular dystrophy. We show here that patients affected by limb-girdle muscular dystrophy 2D (LGMD2D, characterized by -sarcoglycan deficit) have a reduction of this subset of pericytes and hence mesoangioblast could not be derived for cell therapy. Therefore, we reprogrammed LGMD2D fibroblasts and myoblasts to induced pluripotent stem cells (iPSCs) and developed a protocol for the derivation of mesoangioblast-like cells from them. These cells can be expanded and genetically corrected with a muscle-specific lentiviral vector expressing human -sarcoglycan. Upon transplantation into ad hoc generated -sarcoglycan-null immunodeficient mice, they generate myofibers expressing -sarcoglycan. This approach may be useful for muscular dystrophies that show a reduction of resident progenitors and provides evidence of pre-clinical safety and efficacy of disease-specific iPSCs.

Publication Title

Transplantation of genetically corrected human iPSC-derived progenitors in mice with limb-girdle muscular dystrophy.

Sample Metadata Fields

Sex, Specimen part

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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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