Transcription profiling of Icsbp (Irf-8) deficient mice
ABSTRACT: In order to study the consequences of the loss of Icsbp expression in hematopoiesis Granulocyte-Monocyte Progenitors from bone marrow were isolated from Icsbp wild type and deficient mice by flow cytometry. Global gene expression was performed using Affymetrix gene chip technology. Experiment Overall Design: GMP from Icsbp wild type and deficient mice were isolated as described by Terszowski et al. (Blood. 2005 Mar 1;105(5):1937-45). Wild type GMP were prepared from two independent biological replica using pooled bone marrow from alt least 10 independent mice. The first was analyzed using the Affymetrix MOE 430A and the second using MOE430_2. GMP from Icsbp deficient mice were prepared from three independent biological replica from at least 8 individual mice. The first two samples were analyzed using the Affymetrix MOE 430A and the third using MOE430_2.
Project description:Monocytes and macrophages express an extensive repertoire of G Protein-Coupled Receptors (GPCRs) that regulate inflammation and immunity. In this study we performed a systematic microarray analysis of GPCR expression in primary mouse tissues to identify family members that are either enriched in macrophages compared to a panel of other cell types, or are regulated by an inflammatory stimulus, the bacterial product lipopolysaccharide (LPS). Experiment Overall Design: Multiple tissues were taken from naïve male C57BL6 mice for hybridization to MOE430_2 arrays
Project description:Deletion of AMPK significantly extended the onset of leukemogenesis and depleted leukemia initiating cells (LICs). To identify how AMPK regulates LICs, we performed gene expression profiling of LICs isolated from AMPK wild type leukemic mice or AMPK-deficient leukemic mice. 4 groups were analyzed; 1) Whole leukemia (GFP+) from AMPK WT ( AMPKfl/fl) mice, 2) Whole leukemia (GFP+) from AMPK-deficient ( AMPKΔ/Δl) mice, 3) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK WT ( AMPKfl/fl) mice, 4) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK-deficient ( AMPKΔ/Δl) mice.
Project description:Mouse Iron Distribution Dynamics
Dynamic model of iron distribution in mice. This model attempts to fit the radioiron tracer data from Lopes et al. 2010 for mice fed iron deficient and rich diets by adjusting the rate of iron intake (vDiet) and the hepcidin synthesis rate (vhepcidin) independently for each experiment. All other parameters are those that provide the best fit for the adequate diet.
This model includes the radioiron tracer species.
Differences in parameter values between deficient, rich, and adequate diets:
Project description:This project investigates the function of p68/p72 in muscle gene expression and skeletal C2C12 cell differentiation. p68/p72 in C2C12 cells cultured in either growth medium (GM) or differentiation medium (DM) was knocked down using shRNA p68/p72 retrovirus, and globle gene expression was profiled using Affymetrix MOE 430A and 430B GeneChip. Experiment Overall Design: The specific aim is to study muscle gene expression changes and skeletal muscle differenciation using RNA interference of p68/p72 in C2C12 cells.
Project description:To understand the mechanism underlying Mo and DC development Overall design: Murine GMP, CDP, pre-cDC, Ly6C+ Mo, CD4+ cDC, CD8+ cDC and Neu were isolated from wild-type or IRF8-deficient mice.
Project description:Using wild type mice and mice deficient for STING, we compared genome-wide expression of RNA in response to STING activation with DMXAA Overall design: To look for the role of STING-mediated pathway in activation of T cells, we activated naïve T cells with DMXAA, a synthetic agonist of STING, together with activation of TCR. To define a STING-specific effect, STING-deficient animals were used as a control. We isolated naïve T cells from peripheral lymph nodes, negatively selected them using magnetic beads coated with antibodies, and activated cells for 4 hours in specified conditions. Next, we isolated RNA and made library using TruSeq kit (Illumina) for the library construction.One replica of each sample is provided
Project description:Using wild type mice and mice deficient for either IFNb1 or IFN-receptor, we analysed the effect of the constitutive IFN on genome-wide expression Overall design: To look for the role of constitutive interferon, we compared levels of expression of Interferon-stimulated genes (ISGs) in alveolar macrophages or liver in three mouse lines that is, C57BL6, IFNb1-KO, and IFN-receptor KO mice. Specifically, we isolated RNA from rested alveolar macrophages or liver and made library using Illumina TruSeq kit for the library construction. One replica of each sample is provided.
Project description:Using mice deficient for several genes that contribute to constitutive levels of type I interferon, we compared genome-wide expressionof RNA in rested macrophages of these mice. Overall design: To look for the role of constitutive interferon, we matured bone marrow derived macrophages from different mouse strains including strains with deficiency for IFNAR (interferon receptor) and STING (Stimulator if Interferon Genes) and compared levels of expression of Interferon-stimulated genes (ISGs). One replica of each sample is provided
Project description:Transcriptional response of Bacillus subtilis to moenomycin in wild-type 168. Bacillus subtilis 168, WT (-MOE) vs. WT (+MOE). The experiment was conducted in triplicate using three independent total RNA preparations. Untreated samples were labeled with Alexa Fluor 555 and moenomycin treated samples were labeled with Alexa Fluor 647.
Project description:Mouse Iron Distribution Dynamics
Dynamic model of iron distribution in mice. This model includes only normal iron with the parameters that fit the data from Lopes et al. 2010 for mice fed a deficient iron diet.
This model does not include the radioiron tracer species. It is appropriate to study the properties in conditions where no tracers are used (for example for steady state analysis).