To identify genes regulated by Rx3 during optic vesicle morphogenesis, adult zebrafish carriers of a null rx3 mutation were mated. Before 13 hours post fertilization (hpf), the earliest time point at which optic vesicle evagination phenotypes could be reliably detected, offspring were phenotypically separated into pools comprising of mutants with an absence of optic vesicles or siblings exhibiting a wild-type phenotype. Three replicates of pooled RNA samples from 13 hpf eyeless mutants (rx3-/-) or phenotypically wild-type siblings (rx3+/+ or rx3+/-), and one replicate of 13 hpf wild-type zebrafish larva were collected for whole transcriptome sequencing. Overall design: Whole transcriptome sequencing (RNA-seq) was performed on zebrafish rx3-/- mutants, wild-type siblings and wild-type AB strains at 13 hpf
Genes and signaling networks regulated during zebrafish optic vesicle morphogenesis.
No sample metadata fields
View SamplesGM-CSF positve CD4 cells are found at sites of inflammation. The purpose of this study was to understand their transcriptional profile relative to known Th1 and Th17 subsets. Overall design: Human CD4 T cells were isolated by magnetic negative selection and activated with PMA and ionomycin. A cytokine capture assay was used to isolate CD45RA-positive, cytokine negative, IFN-gamma-single-positive, IL-17A-single-positive, GM-CSF-single positive and IL-17A-GM-CSF-double positive cells.
Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis.
Specimen part, Subject
View SamplesInterstitial cells of Cajal (ICC) are electrical pacemakers and mediators of neuromuscular neurotransmission in the gastrointestinal tract. Gastrointestinal stromal tumors (GIST) arise within the ICC lineage due to activating KIT/PDGFRA mutations. In this study we developed a method for isolation of human ICC by immunolabeling and fluorescence-activated cell sorting (FACS). Briefly, human gastric musculature was dissociated and incubated with antibodies against CD45, FCER1A, CD11B, KIT, and CD34. ICC (defined as HP-KIT+CD34- cells), NOT ICC (defined as HP-KIT-CD34- cells), and hematopoietic (HP) cells (defined as HP+ cells) were isolated using FACS. Microarray was performed on ICC, NOT ICC, HP+ cells, and unfractionated gastric tunica muscularis. This study utilized micorarray for the phenotypic characterization of FACS-sorted human ICC, allowing comparison of ICC to other cells of the gastric musculature, including GIST.
Hedgehog pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI-mediated activation of KIT expression.
Specimen part
View SamplesTCDD increased expression of numerous differentiation specific genes and decreased expression of numerous genes involved in mitochondrial health and redox homeostasis
2,3,7,8-Tetrachlorodibenzo-p-dioxin-mediated production of reactive oxygen species is an essential step in the mechanism of action to accelerate human keratinocyte differentiation.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptional blood signatures distinguish pulmonary tuberculosis, pulmonary sarcoidosis, pneumonias and lung cancers.
Sex, Specimen part, Disease, Disease stage, Treatment, Race, Subject
View SamplesThis study used whole blood transcriptional signatures from patients with tuberculosis compared to those with similar pulmonary diseases, sarcoidosis, pneumonia and primary lung cancer. TB and sarcoidosis had similar signatures that were distinct from pneumonia and lung cancer.
Transcriptional blood signatures distinguish pulmonary tuberculosis, pulmonary sarcoidosis, pneumonias and lung cancers.
Sex, Specimen part, Disease, Disease stage, Race
View SamplesThe goal of this study was to determine the transcriptional changes associated with breast cancer cells undergoing vascular mimicry in a 3D assay. Two breast cancer cell lines were plated on matrigel in the presence or absence of serum. MDA-MB-231 cells undergo vascular mimicry on matrigel in the absence of serum, MDA-MB-453 cells do not. Overall design: Four samples were analyzed. MDA-MB-231 and MDA-MB-453 cells were plated for 24 hours on matrigel in the presence or absence of serum. MDA-MB-231 cells undergo vascular mimicry when plated on matrigel in the absence of serum, while MDA-MB-453 cells do not.
ZEB1-repressed microRNAs inhibit autocrine signaling that promotes vascular mimicry of breast cancer cells.
No sample metadata fields
View SamplesThese E. coli strains were grown with various signaling molecules and the expression profiles were determined.
Global effects of the cell-to-cell signaling molecules autoinducer-2, autoinducer-3, and epinephrine in a luxS mutant of enterohemorrhagic Escherichia coli.
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View SamplesEnterohemorrhagic E. coli (EHEC) colonizes the large intestine and causes attaching and effacing lesions (AE). Most of the genes involved in the formation of AE lesions are encoded within a chromosomal pathogenicity island termed the Locus of Enterocyte Effacement (LEE). The LysR-like transcriptional factor QseA regulates the LEE by binding directly to the regulatory region of ler. Here, we performed transcriptome analyses comparing WT EHEC and the isogenic qseA mutant in order to elucidate the extent of QseAs role in gene regulation in EHEC. The following results compare genes that were up-regulated and down-regulated ! 2-fold in the qseA mutant strain compared to the WT strain. At mid-exponential growth, 222 genes were up-regulated and 1874 were downregulated. At late-exponential growth, a total of 55 genes were up-regulated and 605 genes were down-regulated. During mid-exponential growth, QseA represses its own transcription, whereas during late-logarithmic growth, QseA activates expression of the LEE genes as well as non-LEE encoded effector proteins. During both growth phases, several genes carried in O-islands, were activated by QseA, whereas genes involved in cell metabolism were repressed. We also performed electrophoretic mobility shift assays, competition experiments, and DNAseI footprints, and the results suggested that QseA directly binds both the ler proximal and distal promoters, its own promoter, as well as promoters of genes encoded in EHEC-specific O-islands. Additionally, we mapped the transcriptional start site of qseA, leading to the identification of two promoter sequences. Taken together, these results indicate that QseA acts as a global regulator in EHEC, coordinating expression of virulence genes.
The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7.
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View SamplesBacterial pathogens must be able to both recognize suitable niches within the host for colonization and successfully compete with commensal flora for nutrients in order to establish infection. Ethanolamine (EA) is a major component of mammalian and bacterial membranes and may be used by pathogens as a carbon and/or nitrogen source in the gastrointestinal tract. We examined how EA influences gene expression in the human pathogen enterohemorrhagic Escherichia coli O157:H7 (EHEC). Our results indicate EA is not only important for nitrogen metabolism, but that EA is used in cell-to-cell signaling to activate virulence gene expression. Genes encoding for the global regulatory proteins QseC, QseE, and QseA, as well as for attaching and effacement (AE) lesion formation and Shiga toxin are differentially regulated when EHEC is grown with micromolar concentrations of EA. We also constructed a deletion of eutR that encodes the regulator of the eut (EA utilization) operon and examined virulence gene expression. These results suggest that EutR is important in regulating gene expression in response to EA, but that EA signaling does not occur solely through EutR. This is the first report linking EA to cell-to-cell signaling and pathogenesis.
Ethanolamine controls expression of genes encoding components involved in interkingdom signaling and virulence in enterohemorrhagic Escherichia coli O157:H7.
No sample metadata fields
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