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accession-icon GSE60369
Myb permits multilineage airway epithelial cell differentiation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 R2 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Myb permits multilineage airway epithelial cell differentiation.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE60365
Effects of Myb shRNA on Airway Epithelial Cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 R2 expression beadchip

Description

The epithelium of the pulmonary airway is specially differentiated to provide defense against environmental insults, but also subject to dysregulated differentiation that results in lung disease. The current paradigm for airway epithelial differentiation is a one-step program whereby a p63+ basal epithelial progenitor cell generates a ciliated or secretory cell lineage, but the cue for this transition and whether there are intermediate steps is poorly defined. Here we identify transcription factor Myb as a key regulator that permits early multilineage differentiation of airway epithelial cells. Myb+ cells were identified as p63 and therefore distinct from basal progenitor cells, but were still negative for markers of differentiation.

Publication Title

Myb permits multilineage airway epithelial cell differentiation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE10211
Airway Epithelial Cell Response to Sendai virus infection
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Oligonucleotide microarrays were used to establish a profile for gene expression in wild-type airway epithelial cells after paramyxoviral infection.

Publication Title

Airway epithelial versus immune cell Stat1 function for innate defense against respiratory viral infection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE37693
Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Primary culture airway epithelial cells, grown under physiologic air-liquid interface conditions, with, or without IL-13 in order to study the effects of this cytokine on mucous cell metaplasia, an important feature of asthma and COPD.

Publication Title

IL-13-induced airway mucus production is attenuated by MAPK13 inhibition.

Sample Metadata Fields

Specimen part

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accession-icon GSE65067
Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease

Publication Title

TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE38668
Translational profiling of hypocretin neurons identifies Lhx9 as necessary for normal development of the hypocretinergic system.
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The immense molecular diversity of neurons challenges our ability to deconvolve the relationship between the genetic and the cellular underpinnings of neuropsychiatric disorders. Hypocretin (orexin) containing neurons of the lateral hypothalamus are clearly essential for the normal regulation of sleep and wake behaviors, and have been implicated in feeding, anxiety, depression and reward. However, little is known about the molecular phenotypes of these cells, or the mechanism of their specification. We have generated a Hcrt bacTRAP line for comprehensive translational profiling of these neuronsin vivo. From this profile, we have identified 188 transcripts, as enriched in these neurons, in additions to thousands more moderately enriched or nominally expressed. We validated many of these at the RNA and protein level, including the transcription factor Lhx9. Lhx9 protein is found in a subset of these neurons, and ablation of these gene results in a 30% loss of Hcrt neuron number, and a profound hypersomnolence in mice.This data suggests that Lhx9 may be important for specification of some Hcrt neurons, and the subsets of these neurons may contribute to discrete sleep phenotypes.

Publication Title

Translational profiling of hypocretin neurons identifies candidate molecules for sleep regulation.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP131850
RNAseq of cortex of 6-month old APPPS1 and APPPS1;Apoe-/- mice
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

One of the hallmarks of Alzheimer's disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-ß (Aß) peptide. ApoE influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aß in the brain. In addition to influencing Aß metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1?E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aß morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. Overall design: Assessed the cortical gene expression of 6-month old APPPS1-21;ApoE-/- (n=7) and APPPS1-21 mice (n=6).

Publication Title

ApoE facilitates the microglial response to amyloid plaque pathology.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE3925
Virus Induced Airway Hyperreactivity and Goblet Cell Metaplasia Phenotypic Extremes (CB6F2/J)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Mice representing phenotypic extremes of airway hyperreactivity and goblet cell metaplasia post-Sendai virus infection were identified from a 500 mouse F2 cohort (CB6F2/J). Whole lung RNA from 3 mice at each extreme was analyzed via microarray for gene expression. Subsequent pairwise comparisons between arrays allowed the identification of genes differentially expressed with respect to the disease phenotypes (airway hyperreactivity and goblet cell metaplasia).

Publication Title

Genetic segregation of airway disease traits despite redundancy of calcium-activated chloride channel family members.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE18010
Pathogenicity of a disease-associated human IL-4 receptor allele in experimental asthma
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Polymorphisms in the interleukin-4 receptor chain (IL-4R) have been linked to asthma incidence and severity, but a causal relationship has remained uncertain. In particular, a glutamine to arginine substitution at position 576 (Q576R) of IL-4R has been associated with severe asthma, especially in African Americans. We show that mice carrying the Q576R polymorphism exhibited intense allergen-induced airway inflammation and remodeling. The Q576R polymorphism did not affect proximal signal transducer and activator of transcription (STAT) 6 activation, but synergized with STAT6 in a gene target and tissue-specific manner to mediate heightened expression of a subset of IL-4 and IL-13responsive genes involved in allergic inflammation. Our findings indicate that the Q576R polymorphism directly promotes asthma in carrier populations by selectively augmenting IL-4Rdependent signaling.

Publication Title

Pathogenicity of a disease-associated human IL-4 receptor allele in experimental asthma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE17322
Mouse lung CD103+ and CD11b-high dendritic cell (DC) subsets
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mouse lung CD11c+ dendritic cells are composed of 2 major DC subsets, the CD103+CD11b-low/intermediate DC (CD103+ DC) and the CD11b-highCD103- DC (CD11b-high DC). These 2 subsets are functionally distinct. Comparison of their functions showed CD103+ DC

Publication Title

Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8alpha+ conventional dendritic cells.

Sample Metadata Fields

Specimen part

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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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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