This SuperSeries is composed of the SubSeries listed below.
Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.
Specimen part
View SamplesThe aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.
Macrophage migration inhibitory factor: a central regulator of wound healing.
Sex, Age, Specimen part, Subject
View SamplesA study to define the binding loci of RelA-containing NF-kappaB dimers and subsequent correlation with gene expression in a human myometrial smooth muscle cell line after exposure to TNF.
Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic profiling of CHEK2*1100delC-mutated breast carcinomas.
Specimen part
View SamplesOne of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner. Overall design: Sorted splenic dendritic cell subsets from either Flt3+/+ or Flt3ITD/+ mice were sequenced for mRNA profiling. For each subset per genotype contains 2-3 replicates, all from independent experiments.
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.
Specimen part, Cell line, Subject
View SamplesExtrahepatic bile ducts were isolated from mouse pups at days 0-3 and primary cholangiocytes were isolated. Cholangiocytes were treated with DMSO, bilatresone (TOX4), betavulgarin (TOX2), and isoflavanone (TOX3), as per Lorent et al, Science Translationa Medicine 2015;286:286ra67 (Fig. 1), all in DMSO. Treatment concentrations were 2.0 micrograms/ml, for 6 hours.
Extrahepatic cholangiocyte obstruction is mediated by decreased glutathione, Wnt and Notch signaling pathways in a toxic model of biliary atresia.
Treatment
View SamplesThis study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model. Overall design: 3' RNA-Seq (QuantSeq) profiling of ColVIcre+ wt and MyD88 knockout primary mouse intestinal mesenchymal cells before and after treatment with LPS for 6 hours. 3 replicates per group.
Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis.
Specimen part, Cell line, Treatment, Subject
View SamplesGene expression analysis of purified KitL-tomato+ and KitL-tomato- thymic vascular endothelial cells, cortical and medullary thymic epithelial cells from 5 weeks old male kitL-tomato reporter mice Overall design: Differentially expressed genes analysis of thymic stromal cells
A dynamic niche provides Kit ligand in a stage-specific manner to the earliest thymocyte progenitors.
No sample metadata fields
View SamplesWe sequenced liver mRNA isolated from biliatresone-treated zebrafish larvae and DMSO-treated controls in order to elucidate the molecular pathways induced by biliatresone, a biliary toxin that is responsible for outbreaks of biliary atresia in Australian liverstock. Overall design: Liver mRNA profiles of biliatresone-treated zebrafish larvae and DMSO-treated controls were generated by deep sequencing, in duplicates.
Glutathione antioxidant pathway activity and reserve determine toxicity and specificity of the biliary toxin biliatresone in zebrafish.
No sample metadata fields
View SamplesObesity increases colorectal cancer despite other disturbances. We have used the AOM/DSS protocol to induce colitis-associated cancer in control and IL-6Ra deficient animals. Tumours were microdissected and globalgene expression was analysed using microarray.
Obesity exacerbates colitis-associated cancer via IL-6-regulated macrophage polarisation and CCL-20/CCR-6-mediated lymphocyte recruitment.
Sex, Age, Specimen part
View Samples