Project description:Myeloid leukemia cell lines HL60, THP-1, and U937 undergo macrophage-like differentiation after treatment with phorbol ester. To explore genes whose exon usage was altered during macrophage differentiation, we compared exome of PMA-treated (differentated) and vehicle-treated (undifferentiated) myeloid cell lines. HL60, THP-1, and U937 cells were treated with either phorbol 12-myristate 13-acetate (PMA,30nM) or its vehicle (DMSO) for 3 days, and subjected to exome analysis using Affymetrix human exon 1.0ST arrays.
Project description:Myeloid leukemia cell lines HL60, THP-1, and U937 undergo macrophage-like differentiation after treatment with phorbol ester. To explore genes whose exon usage was altered during macrophage differentiation, we compared exome of PMA-treated (differentated) and vehicle-treated (undifferentiated) myeloid cell lines.
Project description:So far, we have found phorbol 12-myristate 13-acetate (PMA) induced ubiquitin specific peptidase (USP) 2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. HL60, THP-1, and U937 undergoes differentiation into macrophage-like cells after stimulation with phorbol ester. To explore molecular function of USP2 in macrophages especially during lipopolysaccharide(LPS) response, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA.
Project description:So far, we have found phorbol 12-myristate 13-acetate (PMA) induced ubiquitin specific peptidase (USP) 2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. HL60, THP-1, and U937 undergoes differentiation into macrophage-like cells after stimulation with phorbol ester. To explore molecular function of USP2 in macrophages especially during lipopolysaccharide(LPS) response, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA.
Project description:So far, we have found PMA induced USP2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. To explore molecular function of USP2 in the cells, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA.
Project description:So far, we have found PMA induced USP2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. To explore molecular function of USP2 in the cells, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA. HL60 derivatives continuously expressing shRNA for USP2 and control shRNA were treated with PMA (30nM) for 0, 1, 2, and 3 days. Total RNA was extracted from the cells and subjected to microarray experiments using Human Genome U133 GeneChips.
Project description:Analysis of interferon-stimulated genes (ISGs) in various primary cells and immortalized cell lines, following type 1 interferon (IFN) treatment. Some cell types become resistant to HIV-1 infection following type 1 interferon treatment (such as macrophages, THP-1, PMA-THP-1, U87-MG cells and to a lesser extent, primary CD4+ T cells) while others either become only partially resistant (e.g., HT1080, PMA-U937) or remain permissive (e.g., CEM, CEM-SS, Jurkat T cell lines and U937); for more information see (Goujon and Malim, Journal of Virology 2010) and (Goujon and Schaller et al., Retrovirology 2013). We hypothesized that the anti-HIV-1 ISGs are differentially induced and expressed in restrictive cells compared to permissive cells and performed a whole genome analysis following type 1 IFN treatment in cell types exhibiting different HIV-1 resistance phenotypes.
Project description:Analysis of interferon-stimulated genes (ISGs) in various primary cells and immortalized cell lines, following type 1 interferon (IFN) treatment. Some cell types become resistant to HIV-1 infection following type 1 interferon treatment (such as macrophages, THP-1, PMA-THP-1, U87-MG cells and to a lesser extent, primary CD4+ T cells) while others either become only partially resistant (e.g., HT1080, PMA-U937) or remain permissive (e.g., CEM, CEM-SS, Jurkat T cell lines and U937); for more information see (Goujon and Malim, Journal of Virology 2010) and (Goujon and Schaller et al., Retrovirology 2013). We hypothesized that the anti-HIV-1 ISGs are differentially induced and expressed in restrictive cells compared to permissive cells and performed a whole genome analysis following type 1 IFN treatment in cell types exhibiting different HIV-1 resistance phenotypes. 48 samples; design: 9 cell lines, primary CD4+ T cells and primary macrophages, untreated and IFN-treated; 2 replicate experiments per cell line; 3 replicate experiments per primary cell type