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Platform
GSE81986
Homo sapiens
294 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A formalin-fixed paraffin-embedded (FFPE)-based prognostic signature to predict metastasis in clinically low risk stage I/II microsatellite stable colorectal cancer.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 150 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This study was conducted in order to identify biomarkers for a prognostic gene expression signature for metastases in early stage CRC.
Publication Title
A formalin-fixed paraffin-embedded (FFPE)-based prognostic signature to predict metastasis in clinically low risk stage I/II microsatellite stable colorectal cancer.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Transcriptome analysis of RNAs extracted from 2 hour-TGF-b-treated or untreated LX-2 cells with or without STAT3 knockdown
Publication Title
Transforming Growth Factor-β (TGF-β) Directly Activates the JAK1-STAT3 Axis to Induce Hepatic Fibrosis in Coordination with the SMAD Pathway.
Sample Metadata Fields
Treatment, Time
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
In order to identify the developmental changes controlling the switch from disease susceptibility to resistance, we performed global gene expression analysis on non-infected and infected intestinal tissues taken from 4-day- and 7-day-old animals.
Publication Title
Maturation of paneth cells induces the refractory state of newborn mice to Shigella infection.
Sample Metadata Fields
Age
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Transcriptome analysis of RNAs extracted from livers of wild type or Smurf1 knock out (KO) or Smurf2 KO mice at age of 11 month old.
Publication Title
Non-proteolytic ubiquitin modification of PPARγ by Smurf1 protects the liver from steatosis.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Illumina HiSeq 2500
Description
The pulmonary alveolar epithelium which play key role in lung biological function is mainly composed of two types of epithelial cells: alveolar type I (AT1) and type II (AT2) cells. We know very little about developmental heterogeneity of the AT1 cell population. By using 10X genomics “Chromium Single Cell” technology, we performed single-cell RNA-seq (scRNA-seq) analyses of AT1 cells at postnatal day 3 (P3), P15, and P60, along with AT2 cells (P60) in mice. Our study identified a robust new genetic marker (Igfbp2) of postnatal AT1 cells. The study also provided the transcriptome information of AT1 cells during alveologensis. Overall design: We performed 10X genomics single-cell RNA-seq at various developmental stages of AT1 cells of lungs at postnatal (P)3, P15, and P60. We also performed 10X genomics single-cell RNA-seq of AT2 cells of P60 lungs.
Publication Title
Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Danio rerio
- 18 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Adult zebrafish can completely regenerate their caudal fin following amputation. This complex process is initiated by the formation of an epithelial would cap over the amputation site by 12 hours post amputation (hpa). Once the cap is formed, mesenchymal cells proliferate and migrate from sites distal to the wound plane and accumulate under the epithelial cap forming the blastemal structure within 48 hpa. Blastemal cells proliferate and differentiate, replacing the amputated tissues, which are populated with angiogenic vessels and innervating nerves during the regenerative outgrowth phase which is completed around 14 days post amputation (dpa). Regenerative outgrowth does not occur in TCDD-exposed zebrafish. To identify the molecular pathways that are perturbed by TCDD exposure, male zebrafish were i.p. injected with 50 ng/g TCDD or vehicle and caudal fins were amputated. Regenerating fin tissue was collected at 1, 3 and 5 dpa for mRNA abundance analysis. Microarray analysis and quantitative real time PCR revealed that wound healing and regeneration alone altered the expression of nearly 900 genes by at least two fold between 1 and 5 dpa. TCDD altered the abundance of 370 genes at least two fold. Among these, several known aryl hydrocarbon responsive genes were identified in addition to several genes involved in extracellular matrix composition and metabolism. The profile of misexpressed genes is suggestive of impaired cellular differentiation and extracellular matrix composition potentially regulated by Sox9b.
Publication Title
Regenerative growth is impacted by TCDD: gene expression analysis reveals extracellular matrix modulation.
Sample Metadata Fields
Sex, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The recent interest in the role of bone marrow derived endothelial progenitor cells in the benefits of estrogen on cardiovascular health brought us to evaluate if estrogen could affect cardiac repair more broadly by regulating biological processes involved in the functional organization of the bone marrow stem cell niche.
Publication Title
Estrogen-induced gene expression in bone marrow c-kit+ stem cells and stromal cells: identification of specific biological processes involved in the functional organization of the stem cell niche.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
MECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of conditional MECP2 overexpression and genetic rescue mice were generated by deep sequencing, in triplicate, using Illumina TruSeq.
Publication Title
Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina HiSeq 2000
Description
MECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of WT, MECP2-TG and MECP2-TG ASO-treated treated mice 8 weeks after the initiation of the treatment, were generated by deep sequencing, in triplicate, using Illumina TruSeq.
Publication Title
Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.
Sample Metadata Fields
No sample metadata fields
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