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accession-icon SRP145447
Commensal Microbiota Promote Lung Tumorigenesis via ?d T Cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Lung cancer is closely associated with chronic inflammation, but the mechanism underlying such inflammation has not been clearly defined. The lung is a mucosal tissue colonized by a diverse bacterial community at the steady state, and pulmonary infections commonly present in lung cancer patients are linked to clinical outcomes. Here we provide evidence that local microbiota provoke inflammation associated with lung adenocarcinoma by activating lung-resident gamma-delta T cells. Germ-free or antibiotic-treated mice were significantly protected from lung tumor initiation and progression induced by Kras mutation and p53 loss. Mechanistically, commensal bacteria stimulated My88-dependent IL-1beta and IL-23 production from myeloid cells, inducing proliferation and activation of V?6+Vd1+ ?d T cells that produced IL-17 and other effector molecules to promote inflammation and tumor cell proliferation. Our findings provide a clear link between local microbiota-immune crosstalk and lung tumorigenesis, and thereby define key cellular and molecular mediators that may serve as effective targets in lung cancer treatment and prevention. Overall design: ?dT cells were isolated from tumor-bearing lungs or spleens of KP mice. Their transcriptional profiles are compared with RNA-seq.

Publication Title

Commensal Microbiota Promote Lung Cancer Development via γδ T Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE40438
Gene expression profiling of resistant and vulnerable motor neuron subtypes in amyotrophic lateral sclerosis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A consistent clinical feature of amyotrophic lateral sclerosis (ALS) is the sparing of eye movements. Pathological studies have confirmed that there is relative sparing of the cranial motor nuclei of the oculomotor, trochlear and abducens nerves, although pathological changes resembling those seen in anterior horn cells are present to a lesser degree. The aim of the present study is to combine LCM and microarray analysis to study the differences between motor neurons that are selectively resistant (oculomotor neurons) and those that are vulnerable (lumbar spinal motor neurons) to the disease process in amyotrophic lateral sclerosis.

Publication Title

Unravelling the enigma of selective vulnerability in neurodegeneration: motor neurons resistant to degeneration in ALS show distinct gene expression characteristics and decreased susceptibility to excitotoxicity.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE145935
Transcriptomic analysis of human astrocytes in vitro reveals hypoxia-induced mitochondrial dysfunction, modulation of metabolism and dysregulation of the immune response
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Changes in the transcriptomic profile of the Sciencell human astrocytes, after hypoxia treatment were compared to control cells receiving no treatment, to identify differentially expressed genes and pathways.

Publication Title

Transcriptomic Analysis of Human Astrocytes In Vitro Reveals Hypoxia-Induced Mitochondrial Dysfunction, Modulation of Metabolism, and Dysregulation of the Immune Response.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE83670
Gene expression profiling of the astrocyte transcriptome in multiple sclerosis normal appearing white matter reveals a neuroprotective role
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling has been performed on astrocytes isolated using laser capture microdissection (LCM) from multiple sclerosis normal appearing white matter (NAWM) and control WM to identify whether specific glial changes exist in NAWM which contribute to lesion development or prevent disease progression

Publication Title

Gene expression profiling of the astrocyte transcriptome in multiple sclerosis normal appearing white matter reveals a neuroprotective role.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE20589
Microarray analysis identifies the gene signature of surviving motor neurons in human SOD1-related motor neuron disease
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling has been performed previously on motor cortex and spinal cord homogenates and of sporadic ALS cases and controls, to identify genes and pathways differentially expressed in ALS. More recent studies have combined the use of laser capture microdissection (LCM) with gene expression profiling to isolate the motor neurons from the surrounding cells, such as microglia and astrocytes, in order to determine those genes differentially expressed in the vulnerable cell population i.e. motor neuron.

Publication Title

Phosphatase and tensin homologue/protein kinase B pathway linked to motor neuron survival in human superoxide dismutase 1-related amyotrophic lateral sclerosis.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE56504
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE33855
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [fibroblasts]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56500
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [LCM]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE19332
Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling has been performed on motor cortex and spinal cord homogenates and of sporadic ALS cases and controls, to identify genes and pathways differentially expressed in ALS. More recent studies have combined the use of laser capture microdissection (LCM) with gene expression profiling to isolate the motor neurons from the surrounding cells, such as microglia and astrocytes, in order to determine those genes differentially expressed in the vulnerable cell population i.e. motor neuron.

Publication Title

Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS).

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE29652
Microarray analysis of the astrocyte transcriptome in the ageing brain: relationship to Alzheimer's pathology and ApoE genotype
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Astrocyte dysfunction impacts their normal function, including neuronal support, thereby contributing to neurodegenerative pathologies including Alzheimer's disease (AD). Therefore to understand the role of astrocytes in the pathogenesis of age-related disorders we analysed the gene expression profile of astrocytes with respect to Alzheimer-type pathology.

Publication Title

Microarray analysis of the astrocyte transcriptome in the aging brain: relationship to Alzheimer's pathology and APOE genotype.

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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