Project description:AKGs enriched transcripts associated with PC-, lyso-PC and PAF metabolism. Moreover, AKGs suppressed interferon response genes. We submit heren three sets of NGS analyses. Experiment 1: We treated mouse adipose tissue macrophages (ATMs) with vehicle (ethanol) or 100 nM alkylglycerols (AKGs) for 18h in vitro. Experiment 2: We treated mouse 3T3-L1 preadipocytes with 1 nM neuropeptide FF (NPFF) for 18 h. Experiment 3: we isolated white adipose tissue from C57Black/6 male mice at 8 weeks of age, and brown adipose tissue from the same mice.
Project description:KYSE510 cells were treated with 100 nM PAF for 24 hours,and then KYSE510 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the gene network of KYSE510 cells regulated by PAF.
Project description:Protein-protein interaction analysis for RNA Polymerase II and its elongation factors including: the PAF Complex, the FACT Complex, casein kinase II, DSIF, and TFIIF. These studies also characterized a number of casein kinase II phosphorylation sites on the subunits of the PAF Complex.
Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Recently, using Agilent cDNA microarray technology, we could demonstrate that the glycosidated APL Ino-C2-PAF inhibited the expression of several genes associated with immune response and inflammation in immortalized keratinocytes HaCaT. Here, we analyzed the impact of Ino-C2-PAF on the gene expression profile of HaCaT cells treated with several pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M). The influence of Ino-C2-PAF on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with 5 M-BM-5M Ino-C2-PAF in the presence of a mixture of pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M) for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition, except for control cells where only two experiments were performed. Control cells were mainly necessary to demonstrate the efficiency of this in vitro inflammation model for keratinocytes.