Filters
Technology
Platform
SRP091366
Mus musculus
506 Downloadable Samples
NextSeq 500
Description
We employed marker-free single-cell RNA-Seq to characterize comprehensive transcriptional profiles of 507 cells from seven stages between embryonic day 11.5 and postnatal day 2.5 during mouse liver development. Our data demonstrated the existence of two types of stem/progenitor cells with distinct molecular patterns during liver development. Both types of cells exhibit heterogeneity of transcriptional program within each cell population, suggesting they be in distinct status of self-renewal, cell proliferation and different sub-stages of differentiation and maturation. In general, our data depicting the dynamic trajectories with transcriptional profiles at single-cell resolution during mouse liver development provides insights into the fate decision and transcriptional control of self-renewal, differentiation and maturation of liver stem/progenitor cells. Overall design: The transcriptomes of 507 single cells from E11.5, E12.5, E13.5, E14.5, E16.5, E18.5 and P2.5 mouse livers were analyzed in this study. ERCC Spike-ins were included in each sample as control. For E11.5 stage, we analyzed 70 single cells from one embryonic mouse (pooled sibling livers); for E12.5 stage, we analyzed 2 biological replicates (2 embryonic mouse), with 83 single cells from replicate 1 and 17 single cells from replicate 2; for E13.5 stage, we analyzed 71 single cells from one embryonic mouse; for E14.5 stage, we analyzed 2 biological replicates, with 75 single cells from replicate 1 and 24 single cells from replicate 2; for E16.5 stage, we analyzed 2 biological replicates, with 56 single cells from replicate 1 and 22 single cells from replicate 2; for E18.5 stage, we analyzed 2 biological replicates, with 39 single cells from replicate 1 and 19 single cells from replicate 2; for P2.5 stage, we analyzed 2 biological replicates, with 21 single cells from replicate 1 and 10 single cells from replicate 2. All single cell samples were processed on the microfluidic system.
Publication Title
Single-cell RNA-Seq analysis reveals dynamic trajectories during mouse liver development.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 32 Downloadable Samples
Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
3T3-L1 adipocytes were treated inhibitors against the glutathione and thioredoxin cycling pools for several time-points (2-24 h).
Publication Title
The transcriptional response to oxidative stress is part of, but not sufficient for, insulin resistance in adipocytes.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
3T3-L1 adipose cells were grown, differentiated and insulin resistance was stimulated by addition of Glucose Oxidase.
Publication Title
The transcriptional response to oxidative stress is part of, but not sufficient for, insulin resistance in adipocytes.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Cross-species gene expression analysis identifies a novel set of genes implicated in human insulin sensitivity.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 38 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Thirty-eight tumors from 17 patients treated with BRAF inhibitor (n=12) or combination BRAF/MEK inhibitors (n=5) with known PD-L1 expression were analyzed. RNA expression arrays were performed on all pre-treatment (PRE, n=17), early during treatment (EDT, n=8) and progression (PROG, n=13) biopsies. HLA-A/HLA-DPB1 expression was assessed by immunohistochemistry (IHC). Gene set enrichment analysis (GSEA) of PRE, EDT and PROG melanomas revealed that transcriptome signatures indicative of immune cell activation were strongly positively correlated with PD-L1 staining. In contrast, MAPK signaling and canonical Wnt/--catenin activity were negatively associated with PD-L1 melanoma expression. The expression of PD-L1 and immune activation signatures did not simply reflect the degree or type of immune cell infiltration, and was not sufficient for tumor response to MAPK inhibition.
Publication Title
PD-L1 Expression and Immune Escape in Melanoma Resistance to MAPK Inhibitors.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Recent discovery reveals HFD insult can cause insulin resistance very rapidly, but the underlying mechanism is still not well understood. We performed a short term experiment in a Diet Induced Insulin resistance mouse model.
Publication Title
Cross-species gene expression analysis identifies a novel set of genes implicated in human insulin sensitivity.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 384 Downloadable Samples
- NextSeq 500
Description
Reversing the dysfunctional T cell state that arises in cancer and chronic viral infections is the focus of therapeutic interventions; however, current therapies are effective in only some patients and some tumor types. To gain a deeper molecular understanding of the dysfunctional T cell state, we analyzed population and single-cell RNA profiles of CD8+ tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activation. This distinct dysfunction module is downstream of intracellular metallothioneins that regulate zinc metabolism and can be identified at single-cell resolution. We further identify Gata-3, a zinc-finger transcription factor in the dysfunctional module, as a regulator of dysfunction, and use CRISPR/Cas9 genome editing to show that it drives a dysfunctional phenotype in CD8+ TILs. Our results open novel avenues for targeting dysfunctional T cell states, while leaving activation programs intact. Overall design: CD8 TILs from WT and MTKO mice were sequenced at single-cell resolution
Publication Title
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 383 Downloadable Samples
- NextSeq 500
Description
Reversing the dysfunctional T cell state that arises in cancer and chronic viral infections is the focus of therapeutic interventions; however, current therapies are effective in only some patients and some tumor types. To gain a deeper molecular understanding of the dysfunctional T cell state, we analyzed population and single-cell RNA profiles of CD8+ tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activation. This distinct dysfunction module is downstream of intracellular metallothioneins that regulate zinc metabolism and can be identified at single-cell resolution. We further identify Gata-3, a zinc-finger transcription factor in the dysfunctional module, as a regulator of dysfunction, and use CRISPR/Cas9 genome editing to show that it drives a dysfunctional phenotype in CD8+ TILs. Our results open novel avenues for targeting dysfunctional T cell states, while leaving activation programs intact. Overall design: CD8 TILs from WT and MTKO mice were sequenced at single-cell resolution
Publication Title
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 384 Downloadable Samples
- NextSeq 500
Description
Reversing the dysfunctional T cell state that arises in cancer and chronic viral infections is the focus of therapeutic interventions; however, current therapies are effective in only some patients and some tumor types. To gain a deeper molecular understanding of the dysfunctional T cell state, we analyzed population and single-cell RNA profiles of CD8+ tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activation. This distinct dysfunction module is downstream of intracellular metallothioneins that regulate zinc metabolism and can be identified at single-cell resolution. We further identify Gata-3, a zinc-finger transcription factor in the dysfunctional module, as a regulator of dysfunction, and use CRISPR/Cas9 genome editing to show that it drives a dysfunctional phenotype in CD8+ TILs. Our results open novel avenues for targeting dysfunctional T cell states, while leaving activation programs intact. Overall design: CD8 TILs from WT and MTKO mice were sequenced at single-cell resolution
Publication Title
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples