Project description:To tease apart the downstream signaling triggered by the Jam3-mediated signaling, Microarray-sequencing analyses were conducted with WT and Jam3-null LICs.The gene ontology (GO) analysis showed that JAM3 might mainly be involved in signal transduction and phosphorylation pathways. KEGG further indicated that JAM3 was required for the Wnt signaling and hematopoietic cell lineage.
Project description:To tease apart the downstream signaling triggered by the Asic3-mediated ion current, RNA-sequencing analyses were conducted with WT and Asic3-null LICs. We found 199 genes were significantly up-regulated, while 587 were down-regulated in Asic3-null LICs. The gene ontology (GO) analysis showed that ASIC3 might mainly be involved in the pattern recognition receptor activity, protein complex binding and calcium ion binding. KEGG further indicated that ASIC3 was required for the glutathione metabolism and hematopoietic cell lineage.
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 ( AMPK?/?l) 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 ( AMPK?/?l) mice.
Project description:To determine the underlying molecular mechanisms that control the homing and self-renewal activities of P2x7-null Mac-1+c-Kit+ LICs, WT and P2x7-null LICs were WT and P2x7-KO were sorted by flow cytometry, followed by the extraction of total RNA and subjected to the RNA-sequencing.
Project description:To determine the underlying molecular mechanisms that control the homing and self-renewal activities of P2x1-null Mac-1+c-Kit+ LICs, WT and P2x1-null LICs were WT and P2x1-KO were sorted by flow cytometry, followed by the extraction of total RNA and subjected to the RNA-sequencing.
Project description:We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2. For WT cells, 3 biological replicates were hybridized. For Ezh2-null cells, 4 biological replicates were hybridized. For Eed-cells, 3 biological replicates were hybridized.