Gene expression in NPM1 wildtype and mutated AML patients with high or low hsa_circ_0075001 expression
Circular RNAs of the nucleophosmin (NPM1) gene in acute myeloid leukemia.
Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Specimen part, Cell line
View SamplesCNS leukemia is still the major obstacle in treating childhood acute lymphoblastic leukemia (ALL). We have used our NOD/SCID/huALL xenotransplantation model to identify molecular pathways leading to the infiltration of leukemic cells into the CNS compartment.
Central nervous system involvement in acute lymphoblastic leukemia is mediated by vascular endothelial growth factor.
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View SamplesTargeted mouse mutants with inactivated Mixed-Lineage-Leukemia-5 (Mll5, MGI:1924825) alleles exhibit numerical, cell cycle and functional abnormalities in their hematopoietic stem and progenitor cell (HSPC) compartments, including hyper-proliferation of otherwise quiescent hematopoietic stem cells, lack of long-term reconstitution potential and profound radiation sensitivity. Most of the HSPC defects are secondary to increased levels of DNA damage and intracellular accumulation of reactive oxygen species (ROS). To obtain first insights into underlying molecular mechanisms, we performed Affymetrix gene chip analysis using total RNA isolated from FACS-sorted Lin-Sca1+Kit+ (LSK) cells of Mll5+/+ and Mll5-/- mice, both with and without prior long-term treatment with the ROS quencher N-Acetyl-L-Cysteine (NAC). As key finding, microarray data revealed elevated hybridization signals for several transcripts of known or putative IFN-1 target genes in LSK cells from Mll5-/- mice irrespective of NAC-treatment. In fact, comprehensive gene set enrichment analysis identified a number of gene sets closely associated with interferon responses that were significantly affected in Mll5-/- LSK cells.
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Specimen part, Treatment
View SamplesMEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model
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Specimen part
View SamplesTotal bone marrow (BM) from miR-223 knockout (mir-223-/-) and wildtype (miR-223+/+) mice 21 was extracted, prestimulated for 2 days. Then, the BM cells were simultaneously cotransduced with MSCV-Hoxa9-pgk-neomycin and a MSCV-Meis1-IRES-YFP by co-cultivation with irradiated (4,000 cGy) viral producers. HoxA9-Meis1 transduced cells were sorted for YFP expression and continuously selected with neomycin (1.4 mg/ml).
Comprehensive analysis of mammalian miRNA* species and their role in myeloid cells.
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View SamplesLamin B1 is a component of the nuclear envelope involved in epigenetic chromatin regulation and is reduced during B cell activation and formation of lymphoid germinal centres. RNAi-mediated reduction of Lamin B1 results in spontaneous SHM as well as kappa-light chain aberrant surface expression showing that Lamin B1 is a negative epigenetic regulator of SHM.
No associated publication
Cell line
View SamplesWe treated 80% confluent J774A.1 macrophages with 1 nM neuropeptide-FF (NPFF) for 18 h.
Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages.
Treatment
View SamplesBcl11b plays an important role in postnatal dentate gyrus development and adult neurogenesis. To determine its role in adult neurogenesis independant from postnatal development the Bcl11b mutation was induced at the age of 2 months.
Stability and Function of Hippocampal Mossy Fiber Synapses Depend on <i>Bcl11b/Ctip2</i>.
Specimen part
View SamplesThe anaphylatoxin C5a is a potent mediator of innate immunity and promotes inflammation via its receptor C5aR1 upon complement system activation danger-associated molecular patterns. Both C5a and C5aR1 are thought to be contributing factors in inflammatory and infectious conditions of the bone. Bone fracture healing, for example, was significantly improved when applying a C5aR1-antagonist in a rodent model of severe systemic inflammation and osteoblasts were found to be target cells for C5a in this setting. Interestingly, osteoblasts up-regulate C5aR1 during osteogenic differentiation and after bone injury. Further, C5a induces inflammatory cytokines, such as IL-6, and the osteoclastogenic mediator RANKL in osteoblasts. However, the molecular mechanisms underlying C5a-C5aR1 signaling axis in osteoblasts remain unclear, and further targets of C5a are still elusive. Using microarray analysis, we analyzed intracellular events following C5aR1 activation in osteoblasts and defined up- or down-regulated genes and their belonging biological pathways.
C5aR1 interacts with TLR2 in osteoblasts and stimulates the osteoclast-inducing chemokine CXCL10.
Treatment
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