Filters
Technology
Platform
SRP140740
Mus musculus
1 Downloadable Sample
Illumina HiSeq 2500
Description
Normal development requires tight regulation of cell proliferation and cell death. Here, we investigated these control mechanisms in the hyaloid vessels, a temporary vascular network in the mammalian eye that requires a Wnt/ß-catenin response for scheduled regression. Transcriptome analysis of the postnatal day 5 mouse hyaloid showed expression of several Wnt pathway proteins. We investigated whether the hyaloid Wnt response was linked to the oncogene Myc, and the cyclin-dependent kinase inhibitor P21 (CDKN1A), both established regulators of cell cycle progression and cell death. Our analysis showed that the Wnt pathway coreceptors LRP5 and LRP6 have overlapping activities mediating the Wnt/ß-catenin signaling in hyaloid vascular endothelial cells (VECs). We also showed that both Myc and Cdkn1a are downstream of the Wnt response and are required for hyaloid regression but for different reasons. Conditional deletion of Myc in VECs suppressed both proliferation and cell death. By contrast, conditional deletion of Cdkn1a resulted in VEC over-proliferation that countered the effects of cell death on regression. When combined with analysis of MYC, and P21 protein levels, this analysis suggests that a Wnt/ß-catenin, MYC-P21 pathway regulates scheduled hyaloid vessel regression. Overall design: Hyaloid vascular preparations from postnatal day 5 mice were harvested in cold PBS and RNA extracted in Tri Reagent. RNA amplifcation was performed on total RNA before cDNA library was made. Samples were then sequenced using Illimina HiSeq2500 to obtain 25-30 million paired-end reads.
Publication Title
Developmental vascular regression is regulated by a Wnt/β-catenin, MYC and CDKN1A pathway that controls cell proliferation and cell death.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of five Notch signaling-dependent human T-ALL cell lines (ALLSIL, DND41, HPBALL, KOPTK1, TALL-1) treated with gamma-secretase inhibitor (GSI) to block Notch signaling. Samples include parental cells, cells rescued by retroviral transduction with ICN (a GSI-independent form of activated Notch1), and cells retrovirally transduced with c-Myc (an important downstream target of Notch1). Results allow segregation of bona fide Notch targets from other genes affected by gamma-secretase inhibition as well as from targets downstream of c-Myc.
Publication Title
High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling.
Sample Metadata Fields
Cell line
View Samples- Mus musculus, Homo sapiens
- 24 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip, Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Defined conditions for the isolation and expansion of basal prostate progenitor cells of mouse and human origin.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Isolation and culture of primary prostate epithelial stem/progenitor cells (PESC) has been proven difficult and ineffective. Here we present methods to grow and expand both murine and human basal PESCs long-term in serum- and feeder-free conditions. The method enriches for adherent mouse basal PESCs with a Lin-Sca1+ CD49f+Trop2high phenotype. Progesterone and sodium selenite are additionally required for the growth of human Lin-CD49f+Trop2high PESCs. The gene expression profiles of expanded basal PESCs show similarities to ES cells and Lamin B1 and PRDX1 were identified as novel PESC markers. If transplanted in combination with urogenital sinus mesenchyme, expanded mouse and human PESCs generate ectopic prostatic tubules demonstrating their stem cell activity in vivo. The novel methods will facilitate the cellular, molecular and genomic characterization of normal and pathologic prostate glands of mouse and human origin.
Publication Title
Defined conditions for the isolation and expansion of basal prostate progenitor cells of mouse and human origin.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip, Illumina MouseWG-6 v2.0 expression beadchip
Description
Isolation and culture of primary prostate epithelial stem/progenitor cells (PESC) has been proven difficult and ineffective. Here we present methods to grow and expand both murine and human basal PESCs long-term in serum- and feeder-free conditions. The method enriches for adherent mouse basal PESCs with a Lin-Sca1+ CD49f+Trop2high phenotype. Progesterone and sodium selenite are additionally required for the growth of human Lin-CD49f+Trop2high PESCs. The gene expression profiles of expanded basal PESCs show similarities to ES cells and Lamin B1 and PRDX1 were identified as novel PESC markers. If transplanted in combination with urogenital sinus mesenchyme, expanded mouse and human PESCs generate ectopic prostatic tubules demonstrating their stem cell activity in vivo. The novel methods will facilitate the cellular, molecular and genomic characterization of normal and pathologic prostate glands of mouse and human origin.
Publication Title
Defined conditions for the isolation and expansion of basal prostate progenitor cells of mouse and human origin.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.
Publication Title
Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Mus musculus
- 20 Downloadable Samples
- Illumina HiSeq 2000
Description
This dataset is part of a study that investigated how the hematopoietic system coordinates the rapid and efficient regeneration of the megakaryocytic lineage during stress scenarios. We found that the phenotypic hematopoietic stem cell (HSC) compartment contains stem-like megakaryocyte-committed progenitors (SL-MkPs), a cell population that shares many features with multipotent HSCs and serves as a lineage-restricted emergency pool for inflammatory insults. This dataset contains single-cell RNA sequencing data of 30 hematopoietic stem and progenitor cells which, in the context of our study, confirmed that MK-specfic transcripts are of highly variable expression in HSCs. The dataset further showed that variations in MK transcript expression in HSCs is not correlated with global transcriptomic rearrangements. Overall design: Murine bone marrow cells were sorted by Lin-cKit+CD150+CD48- (referred to as cd150+ in the following) and Lin-cKit+CD150- (referred to as cd150- in the following). Transcriptomes of 11 cd150- and 9 cd150+ HSCs were determined using QUARTZ, a single-cell RNASeq protocol
Publication Title
Inflammation-Induced Emergency Megakaryopoiesis Driven by Hematopoietic Stem Cell-like Megakaryocyte Progenitors.
Sample Metadata Fields
No sample metadata fields
View Samples