ABSTRACT: Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced human Hs683 cells Hs683 cells infected with shQk-2, shQk-5 and Hs683 cells infected with shGFP as control
Project description:Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes Ink4a/Arf-/- Pten-/- primary mouse astrocytes infected with shQk-1, shQk-2 and infected with shGFP as control
Project description:Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced human Hs683 cells
Project description:Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced human U87 cells together with miR-20a or a scrambled miRNA control (miR-NT)
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced human Hs683 cells together with miR-20a or a scrambled miRNA control (miR-NT)
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced primary mouse Ink4a/Arf-/- Pten-/- astrocytes together with miR-20a or a scrambled miRNA control (miR-NT)
Project description:Human mesenchymal stem cells (hMSCs) were transduced using lentivirus containing the the triple fusion reporter gene fluc-mrfp-ttk. Microarray studies of hMSCs after transduction with the triple reporter genes using lentivirus were performed to study the effects of transduction on stem cell properties using an oligonucleotide human microarray. Transduced cells were sorted by FACS. Cells with high and low signals were ftacrtionated, and gene expression profiles were determined. Experiment Overall Design: In this study, 8 samples were experimentally evaluated. 2 samples were used as the control without undergoing any transduction. 2 samples were transduced with the virus containing only the backbone. 2 samples were transduced with the lentivirus containing the triple reporter and has high MGFP (>10^3), while 2 samples <10^3.
Project description:During acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation. We used microarray to identify the genes that are differentially expressed caused by miR-17-92a over-expression. CD8+ T cells from P14 TCR transgenic mice were infected with miR-17-92a-MSCV-IRES-Thy1.1 vector and transfer to C57BL6 recipients. Chimeras were infected with LCMV Armstrong. Thy1.1+ miR-17-92a-MSCV-IRES-Thy1.1 transduced P14 cells and Thy1.1- non-transduced P14 cells were sorted by FACS. RNA was extracted from samples, labeled, and hybridized to Affymetrix microarrays.
Project description:To investigate the effects of ZIKV infection or ZIKV-NS4B-transduction on the global proteome scale at early stages of hNPC differentiation into neurons, hNPC cells were infected with ZIKV (Asian strain: H/PF/2013; MOI=0.01) or transduced with ZIKV-NS4B or HCV-NS4B and one day later cells were either left under proliferative conditions or neuronal differentiation was induced with ROCK inhibitors treatment and growth factors withdrawals. Five days later samples were harvested and processed for quantitative label-free proteomics.