Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-53916
PROVIDER: PRJNA200974 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens.
2014-02-17 | GSE46229 | GEO
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens. Two condition experiment: wild type vs leukemic; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.
2014-02-17 | E-GEOD-46229 | biostudies-arrayexpress
Project description:T cell acute lymphoblastic leukemia (T-ALL) develops spontaneously in the thymus of LN3 mice and infiltrates secondary organs, including spleen. We found leukemia-associated myeloid cells from the spleens of overtly sick LN3 mice significantly support survival of splenic T-ALL cells, but not tumor-free splenic CD8+ T cells, in vitro. To determine gene signatures induced in T-ALL cells by tumor-supportive myeloid cells, but not induced in wild-type T cells, we transcriptionally profiled primary LN3 T-ALL cells from leukemic mice and T-lineage cells from tumor-free mice, isolated from thymuses and spleens, via RNA-sequencing.
2020-07-22 | GSE150096 | GEO
Project description:ChIP-Seq for H3K4me3 and H3K27me3 in wild type spleens and spleens from mice having deletion of RBP-J in cells of the renin lineage, which results in B-cell leukemia. Examination of 2 different histone modifications in wild type and mutant spleens.
2014-02-17 | E-GEOD-46566 | biostudies-arrayexpress
Project description:Quantitative proteomic analysis of mouse spleens harvested at various time points during infection with wild type and mutant strain.
| MSV000084299 | MassIVE
Project description:Here we compare gene expression profiles between lungs and spleens following LPS in vivo injection into Wild type, lincRNA-Cox2 knockout and lincRNA-Cox2 mutant mice The aim of the experiment is to determine the cis and trans functions for lincRNA-Cox2 following in vivo LPS challenge within the spleen and lung
2018-12-19 | GSE116354 | GEO
Project description:Inflammatory bowel disease is characterized by chronic relapsing idiopathic inflammation of the gastrointestinal tract and persistent inflammation. Studies focusing on the immune-regulatory function of reactive oxygen species (ROS) are still largely missing. In this study, we analyzed an ROS-deficient mouse model leading to colon adenocarcinoma. Colitis was induced with dextran sulfate sodium (DSS) supplied via the drinking water in wild-type (WT) and Ncf1-mutant (Ncf1) B10.Q mice using two different protocols, one mimicking recovery after acute colitis and another simulating chronic colitis. Disease progression was monitored by evaluation of clinical parameters, histopathological analysis, and the blood serum metabolome using 1H nuclear magnetic resonance spectroscopy. At each experimental time point, colons and spleens from some mice were removed for histopathological analysis and internal clinical parameters. Clinical scores for weight variation, stool consistency, colorectal bleeding, colon length, and spleen weight were significantly worse for Ncf1 than for WT mice. Ncf1 mice with only a 7-day exposure to DSS followed by a 14-day resting period developed colonic distal high-grade dysplasia in contrast to the low-grade dysplasia found in the colon of WT mice. After a 21-day resting period, there was still β-catenin-rich inflammatory infiltration in the Ncf1 mice together with high-grade dysplasia and invasive well-differentiated adenocarcinoma, while in the WT mice, high-grade dysplasia was prominent without malignant invasion and only low inflammation. Although exposure to DSS generated less severe histopathological changes in the WT group, the blood serum metabolome revealed an increased fatty acid content with moderate-to-strong correlations to inflammation score, weight variation, colon length, and spleen weight. Ncf1 mice also displayed a similar pattern but with lower coefficients and showed consistently lower glucose and/or higher lactate levels which correlated with inflammation score, weight variation, and spleen weight. In our novel, DSS-induced colitis animal model, the lack of an oxidative burst ROS was sufficient to develop adenocarcinoma, and display altered blood plasma metabolic and lipid profiles. Thus, oxidative burst seems to be necessary to prevent evolution toward cancer and may confer a protective role in a ROS-mediated self-control mechanism.
2019-05-22 | MTBLS593 | MetaboLights
Project description:Both iron homeostasis and erythropoiesis are known to be affected by aging. Iron needs in mammals are met primarily by iron recycling from senescent red blood cells (RBCs), a task chiefly accomplished by red pulp macrophages (RPMs) in the spleen. Given that RPMs continuously process iron, their cellular functions might be susceptible to age-dependent decline, a possibility that has been unexplored to date. In our project, we identified a formation of undegradable iron- and heme-rich extracellular aggregates in the spleens of 10-11-month-old female mice. To better understand the origin of these aggregates, here, we performed: i) protein identification and intrasample quantification (iBAQ) of proteins of magnetically-isolated red pulp macrophages from spleens of two female 8-weeks-old C57BL/6J (maintained on a standard diet) and ii) label-free quantification of proteins of the splenic protein aggregates formed in the mouse spleen 24 hours after intraperitoneal iron dextran injection, using dextran-injected mice as a control. Two 8-week-old C57BL/6J mice per group were analyzed. This dataset is related to the project PXD032900, which describes quanytitative analysis of proteins in aggregates magnetically isolated from spleen of aged (standard or iron-reduced diet) and young mice (standard diet).
2023-02-02 | PXD038660 | Pride
Project description:Comaprison of the gene expression profiles of the spleen between wild type and Brx haploinsuffieint mice Nuclear factor of activated T-cells 5 (NFAT5) is a transcription factor that regulates hyperosmolarity-responsive genes and helps activated T lymphocytes adapt to and discharge their functions in hyperosmolar environments. We report here that the Rho-type guanine nucleotide exchange factor (GEF) Brx is essential for increased NFAT5 expression in response to osmotic stress in lymphoid tissues. Indeed, brx haploinsufficient mice expressed significantly less NFAT5 in their spleens than wild type controls and their splenocytes had a defective response to osmotic stress in vitro. Haploinsufficient mice also had smaller-sized spleens containing fewer splenocytes, as well as a defective immunoglobulin response to ovalbumin compared to wild type mice. The Brx GEF domain and the p38 mitogen-activated kinase (MAPK) cascade were both required for osmotic stress-mediated induction of NFAT5 in Jurkat cells. Brx physically interacted with the cJun kinase (JNK)-interacting protein (JIP) 4, a scaffold protein for activation of the p38 MAPK cascade that was required for osmotic stress-induced NFAT5 expression. Thus, Brx is a signal integrator for the adaptive response to osmotic stress in the immune system, activating small G proteins, attracting JIP4 and stimulating p38 MAPK, ultimately increasing the expression of NFAT5 and activating hyperosmolarity protective genes, a phenomenon crucial for proper immune function in hyperosmolar environments, such as inflammatory sites and immune organs. Keywords: Genetic modification
2009-02-09 | GSE10117 | GEO