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Mus musculus
10 Downloadable Samples
Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The growth factor interleukin-3 (IL-3) promotes the survival and growth of multipotent hematopoietic progenitors and stimulates myelopoiesis. It has also been reported to oppose terminal granulopoiesis and to support leukemic cell growth through autocrine or paracrine mechanisms. We used kinetic microarray, Northern Blotting and bioinformatics analysis of IL-3 dependent myeloblasts to determine whether IL-3 acts in part by regulating the rate of turnover of mRNA transcripts in specific functional pathways. Our results indicate that exposure of myeloblasts to IL-3 causes immediate early stabilization of hundreds of transcripts in pathways relevant to myeloblast function. Examples include transcripts associated with proliferation and leukemic transformation (pik3cd, myb, pim-1), hematopoietic development (cited2), differentiation control (cdkn1a) and RNA processing (BRF1, BRF2). A domain in the 3-utr of IL-6 that mediates IL-3 responsiveness contains AU-rich elements that bind proteins known to modulate mRNA stability, however a known destabilizing protein (AUF1) is shown not to mediate degradation in the absence of IL-3. These findings support a model of IL-3 action through mRNA stability control and suggest that aberrant stabilization of this network of transcripts could contribute to growth patterns observed in leukemia.
Publication Title
IL-3 and oncogenic Abl regulate the myeloblast transcriptome by altering mRNA stability.
Sample Metadata Fields
No sample metadata fields
View Samples- Escherichia coli
- 6 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
E. coli MG155 cells were grown at different grwoth rates in mixed substrate culture. To facilitate different metaoblic status, cells adjust substrate consumption behavior which must be reflected in the gene expression profiles of metablism network. The metabolism network including the substrate transporter systems is our study focus.
Publication Title
Carbon catabolite repression correlates with the maintenance of near invariant molecular crowding in proliferating E. coli cells.
Sample Metadata Fields
Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
Description
We analyzed chromatin dynamics and transcriptional activity of human embryonic stem cell (hESC)-derived cardiac progenitor cells (CPCs) and KDR+/CD34+ endothelial cells generated from cardiogenic or hemogenic mesoderm. Using an unbiased algorithm to hierarchically rank genes modulated at the level of chromatin and transcription, we identified novel candidate regulators of mesodermal lineage determination. HOPX, a non-DNA binding homeodomain protein, was identified as a candidate regulator of blood-forming endothelial cells. We used HOPX reporter and knockout hESCs, as well as hopx loss of function studies in zebrafish, to show the requirement of HOPX in vivo and in vitro in hemato-endothelial lineage specification. Loss of HOPX does not impact endothelial fate specification but markedly reduces primitive hematopoiesis acting at least in part through suppression of Wnt/ß-catenin signaling. Single cell RNA-seq data during mouse hematopoietic development in vivo confirm a role for HOPX in hematopoietic fate. Taken together, we show that HOPX is a novel regulator of hemato-endothelial fate specification in vitro and in vivo that functionally regulates Wnt signaling to modulate primitive hematopoiesis. Overall design: 2 biological replicates were isolated from cardiac progenitor cells (CPCs) and endothelial populations derived from cardiogenic mesoderm (C-ECs) and hemogenic mesoderm (H-ECs). RNA-seq and ChIP-seq (H3K4me3 and H3K27me3) was performed for each replicate.
Publication Title
Single-Cell Transcriptomic Analysis of Cardiac Differentiation from Human PSCs Reveals HOPX-Dependent Cardiomyocyte Maturation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 31 Downloadable Samples
- Illumina HiSeq 2500
Description
Large-scale genome sequencing is poised to provide a substantial increase in the rate of discovery of disease-associated mutations, but the functional interpretation of such mutations remains challenging. Here we show that deletions of a sequence on human chromosome 16 that we term the intestine-critical region (ICR) cause intractable congenital diarrhoea in infants. Reporter assays in transgenic mice show that the ICR contains a regulatory sequence that activates transcription during the development of the gastrointestinal system. Targeted deletion of the ICR in mice caused symptoms that recapitulated the human condition. Transcriptome analysis revealed that an unannotated open reading frame (Percc1) flanks the regulatory sequence, and the expression of this gene was lost in the developing gut of mice that lacked the ICR. Percc1 knockout mice displayed phenotypes similar to those observed on ICR deletion in mice and patients, whereas an ICR-driven Percc1 transgene was sufficient to rescue the phenotypes found in mice that lacked the ICR. Together, our results identify a gene that is critical for intestinal function and underscore the need for targeted in vivo studies to interpret the growing number of clinical genetic findings that do not affect known protein-coding genes. Overall design: Total RNA-seq from dissected regions of the digestive tract, from wild-type and percc1-/- mice.
Publication Title
Noncoding deletions reveal a gene that is critical for intestinal function.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
PAR-1 is known to be involved in the transition from non-metastatic to metastatic melanoma. We sought to determine the downstream target genes regulated by PAR-1 to determine how PAR-1 is contributing to the metastatic melanoma phenotype.
Publication Title
Protease activated receptor-1 inhibits the Maspin tumor-suppressor gene to determine the melanoma metastatic phenotype.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease and a major health problem in the United States. While the cytokine TGF-ß has been implicated in PDAC development, it can exert bot pro- and anti-tumorigenic effects that are highly context dependent and incompletely understood. To better characterize the responses of neoplastic pancreas cells to TGF-ß, three-dimensional (3D) cultures of KrasG12D-expressing mouse pancreatic epithelial cells were employed. While active exposure to exogenous TGF-ß caused the KrasG12D cells to growth arrest, its subsequent removal allowed the cells to enter a hyper-proliferative, quasi-mesenchymal (QM) and progenitor-like state. This transition was highly stable and maintained by autocrine TGF-ß signaling. Transient pulses of TGF-ß have been observed during pancreatitis, a major risk factor for PDAC, and may therefore serve to convert pre-existing KrasG12D-expressing cells into QM cells. While untreated KrasG12D cells formed simple cysts in vivo, QM cells formed ductal structures resembling human PanINs. Furthermore, markers of the QM state are expressed in human PDAC and are associated with worse outcomes. These data suggest that the QM state plays a role in PDAC development and may selectively contribute to more aggressive PDAC subtypes. This work therefore provides novel molecular insights into both PDAC development and the complex role of TGF-ß in tumorigenesis. Overall design: Three technical replicates per experimental group from one isolate were analyzed by RNA sequencing
Publication Title
Pre-neoplastic pancreas cells enter a partially mesenchymal state following transient TGF-β exposure.
Sample Metadata Fields
Subject
View Samples
GSE107088- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Wild-type (WT) miR-378a-3p or edited miR-378a-3p were expressed in SB2 KD-ADAR1 cells to identify the genes regulated by edited miR-378a-3p vs WT miR-378a-3p. PARVA was one of the genes identified to be regulated by edited miR-378a-3p. We demonstrate that this regulation of PARVA is lost in highly metastatic melanoma cells.
Publication Title
A-to-I miR-378a-3p editing can prevent melanoma progression via regulation of PARVA expression.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 31 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Background. Multiple myeloma (MM) cells depend on the bone marrow (BM) niche for growth and survival. However, the tumor genes regulated by the niche are largely unknown.
Publication Title
Niche-modulated and niche-modulating genes in bone marrow cells.
Sample Metadata Fields
Disease, Disease stage, Time
View Samples- Homo sapiens
- 25 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Stimulation of HL60 progenitor cells with either DMSO (1.25% v/v) or atRA (10E-07M) resulted in their differentiation into neutrophils within six days. Gene expression profiles across 12 600 genes were measured for the differentiation processes induced by DMSO and atRA at 0, 2, 4, 8, 12, and 18 h and daily thereafter until day 7 using oligonucleotide DNA microarrays.
Publication Title
Cell fates as high-dimensional attractor states of a complex gene regulatory network.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Gene expression profile (GEP) was analyzed in bone marrow (BM) samples from patients with leukemia or leukemic phase of lymphoma at different time points following aspiration. Among numerous changes in GEP evolved over time a discrete subset of > 60 genes exhibited prompt and sustained switch in expression consistently. Similar results were discovered recently in BM samples from patients with multiple myeloma (GSE36036). GEP was also examined in peripheral blood as well as in BM samples depleted of red blood cells (=WBC) and in cultured cells from some of the patients.
Publication Title
Niche-modulated and niche-modulating genes in bone marrow cells.
Sample Metadata Fields
Specimen part, Disease
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