Project description:The effect of CD151 expression onto the kinome of Jurkat T cells was assessed using kinome analysis. CD151 was expressed in Jurkat T cells by retroviral transduction based on a pMSCV vector. Entrez Gene: 977 UniProtKB: P48509 Jurkat T cells were transduced with the MSCV-CD151 vector and successfully transduced cells were selected using puromycin. For the kinome array experiments 3 independent samples of Jurkat cells and three independent samples of J-CD151 cells were collected. To minimize unspecific background signals, lysates from Jurkat and J-CD151 T cells harvested at different growth stages, which were then pooled to provide one sample prior to loading on the Kinexus antibody microarrays.
Project description:screenning the differentially expressed genes of Jurkat-FF3, Jurkat-miR146a, Jurkat-miR146a-sponge cell lines. To investigate the role of miR-146a on Jurkat T cells, we screened the differentially expressed genes of Jurkat-FF3 (as control), Jurkat-miR146a (as miR-146a overexpression cell line), Jurkat-miR146a-sponge (as miR-146a knock down cell line).
Project description:Ribosome immunoprecipitates of cardiomyocytes isolated from Rpl3l-/- and Rpl3l+/+ mouse hearts were analysed using mass spectrometry.
Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be a potent inducer of apoptosis in various cancer cell lines and primary cancer cells. However, in clinical trials administration of recombinant TRAIL or TRAIL death receptor agonists did not show sufficient efficacy for treatment of tested malignant disorders compared to standard chemotherapy. Acquired resistance of cancer cells to TRAIL and to other âdeath receptorâ ligands may explain not only the inability of TRAIL and TRAIL âdeath receptorâ agonists to achieve the clearance of cancer cells in vivo but also the escape of cancer cells from immune cell â mediated killing. Selective pressure of TRAIL on TRAIL-sensitive Jurkat T-lymphoblastic leukemia cells provided several TRAIL resistant Jurkat cell line clones (TR1, TR2, TR3). We showed that acquired TRAIL resistance was associated with complex disruption of both extrinsic and intrinsic apoptotic pathways manifested by acquired multi-drug resistant phenotype of TR1, TR2, and TR3 clones. To identify changes associated with TRAIL resistance of Jurkat cells we performed genome-wide gene expression analysis of TRAIL-resistant clones (TR) and compared to WT Jurkat cells. We identified significantly increased expression (1.33-fold change with adjusted p < 0.05) of 73 genes in TR1 clone, 53 genes in TR2 clone and 8 genes in TR3 clone, and significant decrease in expression (0.75-fold change with adjusted p < 0.05) of 174 genes in TR1 clone, 36 genes in TR2 clone and 28 genes in TR3 clone. There was an overlap of only 2 significantly overexpressed (midkine / MDK and zinc finger and BTB domain containing 16 gene / ZBTB16 / PLZF) and 4 downregulated genes (YAP1, IGJ, EIF1AY, RPS4Y1) in all three TR clones. Total cellular RNA was isolated from biologic duplicates of untreated Jurkat cells (WT) and TRAIL resistant Jurkat cell line subclones (TR1, TR2, TR3) established by selective pressure of TRAIL 1000 ng/mL on Jurkat cells over the period of 12 weeks.
Project description:Screening the differetial expressed genes with Jurkat-146a(miR-146a over expression),Jurkat-sponge(miR-146a knockdown),Jurkat-FF3(vector control)
Project description:The LEDGF transcript from the PSIP1 gene was knocked down in Jurkat cells using RNAi technology. The resulting Jurkat-derived cell line (Jurkat-siJK2) was compared to a control cell line (wild type Jurkat) using microarray analysis. Genes identified as being modulated by LEDGF were preferential targets of HIV integration. Experiment Overall Design: 2 cell lines were used, Jurkat-siJK2 (experimental) and wild-type Jurkat (control). 3 independent cultures of each cell line were used for independent RNA extractions, labeling reactions and array hybridizations.
Project description:miR-181 is often dysregulated in several types of cancer. This dataset can represent a further insight into gene expression changes and GO Terms associated with miR-181 over-expression. miR-181 was over-expressed in Jurkat cells by transduction with a lentiviral transgenic construct encoding for miR-181 under a PGK promoter. A cognate vector encoding for a control hairpin was used to generate control cell line. mRNA Microarray gene expression profiling of Jurkat cells tranduced with either a miR-181 sponge or control construct. 3 biological replicas have been performed. Note that the control samples are the same as those used in the related experiment E-MTAB-4588