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GSE102046
Homo sapiens
30 Downloadable Samples
Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
We analyzed the transcriptomes of human dendritic cells and macrophages derived from monocytes using MCSF + IL-4 + TNFa, or IL-34 + IL-4 + TNFa, or dendritic cells derived from monocytes using GMCSF + IL-4.
Publication Title
Aryl Hydrocarbon Receptor Controls Monocyte Differentiation into Dendritic Cells versus Macrophages.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
Illumina HiSeq 2500
Description
We performed single-cell RNA-seq on CD14+ monocytes isolated from the blood of healthy donors. Using the 10x chromium technology, we analyzed 425 and 431 cells from 2 individual donors. Overall design: Peripheral Blood Mononuclear Cells (PBMC) were prepared by centrifugation on a Ficoll gradient. Blood CD14+ monocytes were isolated from healthy donors' PBMC by positive selection using magnetic beads. Monocytes were 93-95% CD14+CD16- as assessed by flow cytometry. Cellular suspensions (1700 cells) were loaded on a 10X Chromium instrument (10X Genomics) according to manufacturer's protocol.
Publication Title
Aryl Hydrocarbon Receptor Controls Monocyte Differentiation into Dendritic Cells versus Macrophages.
Sample Metadata Fields
Specimen part, Subject
View Samples- 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
- 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- 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
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 4weeks 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
View Samples