Because niclosamide inhibits growth and progression of endometriotic lesions, we performed RNA-seq in order to identify genes whose expression is regulated by niclosamide in endometriotic lesions. Our results shown that niclosamide modulates several genes related to cell signaling, extracellular matrix, and inflammatory signaling. Overall design: A direct comparison of endometriotic like lesions developed in mice (n=3 per group) treated orally with either vehicle control or 200 mg/kg bw day of niclosamide for 3 weeks.
Niclosamide As a Potential Nonsteroidal Therapy for Endometriosis That Preserves Reproductive Function in an Experimental Mouse Model.
Sex, Specimen part, Cell line, Treatment, Subject
View SamplesThe pig is important for agriculture and as an animal model in human and veterinary medicine, yet, despite over 20 years of effort, it has proved a difficult species from which to generate pluripotent stem cells analogous to those derived from mouse embryos. Here we report the production of LIF-dependent, so called nave type, pluripotent stem cells from the inner cell mass of porcine blastocysts by up-regulating expression of KLF4 and POU5F1. These cells resemble mouse ES cells and are distinct from the FGF2-dependent, induced pluripotent cell type derived from porcine somatic cells.
Leukemia inhibitory factor (LIF)-dependent, pluripotent stem cells established from inner cell mass of porcine embryos.
Sex
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Recombination activating gene-2<sup>null</sup> severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently.
Specimen part
View SamplesIt contains a disruption of the recombination activating gene 2 (RAG2) and homozygoue mice exhibit total inability to initiate V(D)J rearrangement and fail to generate mature T or B lymphocytes. (https://www.taconic.com)
Recombination activating gene-2<sup>null</sup> severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently.
Specimen part
View SamplesIt contains a disruption of the recombination activating gene 2 (RAG2) and homozygoue mice exhibit total inability to initiate V(D)J rearrangement and fail to generate mature T or B lymphocytes. (https://www.taconic.com)
Recombination activating gene-2<sup>null</sup> severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently.
Specimen part
View SamplesIt contains a disruption of the recombination activating gene 2 (RAG2) and homozygoue mice exhibit total inability to initiate V(D)J rearrangement and fail to generate mature T or B lymphocytes. (https://www.taconic.com)
Recombination activating gene-2<sup>null</sup> severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness.
Specimen part, Cell line, Treatment
View SamplesGenome-wide association studies have identified a locus within the second intron of the FGFR2 gene that is consistently the most strongly associated with estrogen receptor-poisive breast cancer risk. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Previously, a systems biology approach was adopted to elucidate the regulatory networks operating in MCF-7 breast cancer cells in order to examine the role of FGFR2 in mediating risk. Here, the same approach has been employed using MCF-7 cells that have been treated with siRNA directed against FGFR2, in order to knock-down FGFR2 expression, to confirm that the differential gene expression that we see when FGF10 signalling is perturbed, on a background of estrogen signalling, is mediated via FGFR2 stimulation.
FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness.
Specimen part, Cell line
View Samples-77-/- mice exhibited late embryonic lethality, anemia, and a constellation of phenotypes. -77 conferred a unique genetic network in myeloid progenitors, endowing progenitors with potential to produce diverse progeny. Overall design: E13.5 WT or -77-/- fetal liver cells were isolated and sorted for common myeloid progenitors (CMPs) defined by Lin-Sca- CD34+FcRlow, and subjected to RNA-sequencing
Cis-regulatory mechanisms governing stem and progenitor cell transitions.
No sample metadata fields
View SamplesLung disease causes most of the morbidity and mortality in cystic fibrosis (CF). However, understanding its pathogenesis has been hindered by lack of an animal model with characteristic features of CF. To overcome this problem, we recently generated pigs with targeted CFTR genes. We now report that within months of birth, CF pigs spontaneously develop hallmark features of CF lung disease including airway inflammation, remodeling, mucus accumulation, and infection. Their lungs contained multiple bacterial species, suggesting an equal opportunity host defense defect. In humans, the temporal and/or causal relationships between inflammation and infection have remained uncertain. To investigate these processes, we studied newborn pigs. Their lungs showed no inflammation, but were less often sterile than controls. Moreover, after intrapulmonary bacterial challenge, CF pigs failed to eradicate bacteria as effectively as wild- type pigs. These results suggest that impaired bacterial elimination is the pathogenic event that initiates a cascade of inflammation and pathology in CF lungs. Finding that CF pigs have a bacterial host defense defect within hours of birth provides an exciting opportunity to further investigate pathogenesis and to test therapeutic and preventive strategies before secondary consequences develop.
Cystic fibrosis pigs develop lung disease and exhibit defective bacterial eradication at birth.
Specimen part
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