Project description:Analysis genes which are elevated after miR10a inhibitor transfection for 24 hours with transfection efficiency more than 95 %inhibition in mesangial cells. The hypothesis is genes which up-regulated significantly can be potential targets for miR-10a in primary human mesangial cells.
Project description:we performed genome-wide transcriptome profiling in mesangial cells and tubular epithelial cells (TECs), which were stimulated by high glucose (HG) and detected the expression of inflammation associated genes. HG increased the mRNA expression of oxidative stress, inflammasome and mammalian target of rapamycin (mTOR) related genes in mesangial cells. Pro-inflammatory/Th1 gene expression was upregulated, but Th2 related gene expression was downregulated in mesangial cells. In TECs, HG stimulation increased pro-inflammatory/Th1/Th2 gene expression. mRNA profiles of human mesangial cells and tubular epithelial cells, which were stimuated HG for 24 hours or mannitol contorol.
Project description:Quiescent human fibroblasts (2091) were transfected with 100nM mature miR-22 RNA duplexes. Cells were collected 24 hours after miR-22 transfection.
Project description:CRISPR KO RNA-seq data: To generate knockouts, we used a commercially available arrayed CRISPR-Cas9 library targeting 81 out of ~100 DUBs and 13 additional proteins in the ubiquitin-proteasome system, including ubiquitin-like proteins; the library was constructed with four, pooled, guides per target. mRNA profiling was performed 96 hours after guide RNA transfection using a high-throughput, low-cost RNA-sequencing method (3’ Digital Gene Expression or 3’DGE-seq) in the MDAMB231 breast cancer cell line. Inhibitor RNA-seq data: For the small molecule inhibitor signatures, MDAMB231 or MCF7 or MCF7 TP53 shRNA breast cancer cells were treated with a panel of DUB inhibitors for 24 hours, then 3'DGE-seq was used to perform the mRNA profiling.
Project description:Activation of GFI1-super-enhancer (GFI1-SE) by a LSD1 inhibitor NCD38 was relevant to myeloid differentiation and antileukemia effect in human erythroleukemia cells (HEL cells). Thus, we investigated the role of GFI1-SE upon NCD38 treatment in HEL cells. We established three independent sublines with bi-allelic deletion of GFI1-SE (CCE2 #114, #141, and #216) using CRISPR-Cas9 genome editing system in HEL cells and a classical limiting dilution method. Control sublines (Ctrl C1, C2, and C5) were established by transfection of parent vector and limiting dilution. After treatment of each subline with DMSO or NCD38 (LSD1i) for 24 hours, these gene expression profiling data were obtained.
