Identification of innate immune responses in the livers of mice infected with liver-stage arresting, transgenic, Plasmodium yoelii parasites. Overall design: Whole liver samples from mock and P. yoelli fabb/f- infected C57BL/6 and BALB/cJ mice. Samples were taken 1 and 3 days post infection
Interferon-mediated innate immune responses against malaria parasite liver stages.
Specimen part, Cell line, Subject
View SamplesElectrochemical gradients of monovalent cations across the plasma membrane (high intracellular potassium, [K+]i vs low intracellular sodium, [Na+]i) are created by the Na+,K+-pump and determine a large variety of physiologically important processes. We hypothesized that transcriptomics changes triggered by hypoxia are at least partially caused by Na+i/K+i-mediated excitation-transcription coupling .
Transcriptomic changes triggered by hypoxia: evidence for HIF-1α-independent, [Na+]i/[K+]i-mediated, excitation-transcription coupling.
Specimen part
View Samplesgene expression data from wild-type and Bcl6-/- regulatory T cells
Bcl6 controls the Th2 inflammatory activity of regulatory T cells by repressing Gata3 function.
Specimen part
View SamplesEndothelin-1 (ET-1) plays a critical role in connective tissue remodeling by fibroblasts during tissue repair and fibrosis. We investigated the molecular pathways in the transmission of ET-1 signals that lead to features of connective tissue remodeling, in particular the role of FAK (focal adhesion kinase).
Inhibition of focal adhesion kinase prevents experimental lung fibrosis and myofibroblast formation.
Specimen part, Treatment
View SamplesWe sought to identify genes regulated by the transcription factor Th-POK (Zbtb7b) in liver Va14i NKT cells, by RNA microarray analysis of global gene expression in Va14i NKT cells from mice homozygous for the Th-POK-inactivating hd point mutation as compared with the same cell population isolated from heterozygous or wild-type age-matched mice.
The transcription factor Th-POK negatively regulates Th17 differentiation in Vα14i NKT cells.
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View SamplesHomeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Specimen part
View SamplesHomeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Specimen part
View SamplesThe TLX1 and TLX3 transcription factor oncogenes play an important role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL)1,2. Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This Systems Biology analysis defined TLX1 and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, network structure analysis of this hierarchical network identified RUNX1 as an important mediator of TLX1 and TLX3 induced T-ALL, and predicted a tumor suppressor role for RUNX1 in T-cell transformation. Consistent with these results, we identified recurrent somatic loss of function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 atop of an oncogenic transcriptional network controlling leukemia development, demonstrate power of network analysis to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor suppressor gene in T-ALL.
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Specimen part, Cell line
View SamplesTransgenic expression of key transcritpion factors inducing T-cell leukemias in mice.
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Specimen part
View SamplesThe experiment was designed in order to knock down the expression of TLX3 gene in T-ALL cell line
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Cell line
View Samples