Gene expression of HSC39 treated with SiRNA targeting TRIM44
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ABSTRACT: We used microarrays to further detail a transcriptional signature of TRIM44 by globally assessing genes that have changes in expression upon knockdown on TRIM44 using two independent SiRNAs targetting the gene (in duplicate) and All Stars Negative siRNA (in quadruplicate) as a control
Project description:We used microarrays to further detail a transcriptional signature of TRIM44 by globally assessing genes that have changes in expression upon knockdown on TRIM44 using two independent SiRNAs targetting the gene (in duplicate) and All Stars Negative siRNA (in quadruplicate) as a control We performed genome-wide comparison of gene expression and identified genes that are differentially expressed in siRNA (targetting TRIM44) treated HSC39 relative to untreated cells, 4 biological replicates per condition
Project description:Investigation of whole genome gene expression level changes in HCT116 cells upon knockdown of Tip60 or p400, compared to control siRNA-transfected cells. Two different siRNA directed against Tip60 were used and experiments were done in duplicate. Same for p400-targetting or control siRNA.
Project description:We used phytochemical profiling techniques to generate a list of compounds present in each of 13 Equisetum arvense samples sourced globally. We used microarrays to detail the global programme of gene expression underlying the treatment of the model system Saccharomyces cerevisiae to a chosen number of these extracts. A thorough bioinformatic analysis was performed to identify the relationship between phytochemical and gene expression response profiles. We analysed 18 Equisetum arvense microarrays. Six samples were chosen from the original 13 for microarray analysis, 5 of which were performed in duplicate and the sixth in quadruplicate. Control arrays were also performed in quadruplicate.
Project description:Bulk RNA-Seq: Gene expression analysis of stromal and tumor fractions of primary and metastatic lesions of polyclonal and monoclonal origin. Primary tumor control samples consist of monoclonal Thy1.1 (no replicates), monoclonal parental (no replicates), monoclonal IL11 (duplicate), monoclonal FIGF (duplicate), and monoclonal CFP (duplicate). Primary polyclonal tumor samples consist of separated Thy 1.1 (duplicate), CFP (no replicates), IL11 (triplicate), and FIGF (triplicate). Metastatic tumor samples consist of monoclonal CFP (duplicate), monoclonal IL11 (quadruplicate), monoclonal FIGF (quadruplicate), monoclonal Thy1.1 (duplicate), and polyclonal samples (duplicate). Metastatic stromal fractions consist of monoclonal CFP (duplicate), monoclonal FIGF (quadruplicate), monoclonal IL11 (quadruplicate), monoclonal parental (duplicate), monoclonal Thy1.1 (duplicate), and polyclonal samples (triplicate). Primary stromal samples consist of monoclonal CFP (duplicate), monoclonal FIGF (duplicate), monoclonal IL11 (duplicate), monoclonal parental (no replicates), monoclonal Thy1.1 (duplicate), and polyclonal samples (triplicate). Further stromal controls consisted of a single fatpad sample and lung sample. Single cell RNA-Seq: Blood, tumors and lungs were isolated from test groups (DOX+ and DOX-) and tumor-naïve animals. Samples were pooled across 3 animals per group, and CD45+populations were FACS-sorted. Two thousand single cells were targeted for each sample.
Project description:Investigation of whole genome gene expression level changes in HCT116 cells upon knockdown of Tip60 or p400, compared to control siRNA-transfected cells. Two different siRNA directed against Tip60 were used and experiments were done in duplicate. Same for p400-targetting or control siRNA. Hybridization experiment using total RNA recovered from independent cell cultures of HCT116 transfected using control, Tip60-targetting or p400-targetting siRNA.
Project description:We designed siRNAs against pyk-reg-90 and pyk-reg-10 using the Dharmacon algorithm (Dharmacon siDESIGN http://www.dharmacon.com/sidesign/). Each of four highest-ranking siRNA sequences for pyk-reg-90 and pyk-reg-10 respectively was tested in our and pyk-reg-90, we used a pool of different siRNAs that included the two most effective siRNAs. The cellsperformance was assessed at 24-hr intervals until 96 hrs posttransfection by qRT-PCR. For both pyk-reg-10resuspended in 1X siRNA buffer (Dharmacon, LaFayette CO, USA) to a stock concentration of 50 ?M. Theexperiments. These siRNAs were were transfected with the corresponding siRNA pool at the final concentration of 100nM and 200nM by using Lipofectamine 2000 (Invitrogen) according to the manufacturer's protocol for further analysis. As control, we used a pool of non-targetting siRNAs (Dharmacon).
Project description:MDA-MB-231 breast carcinoma cells were treated by non-targetting siRNA or siRNAs against EXOSC8. Subsequently, mRNAs from protrusions of the cells were quantified by RNA-seq in presence of Rho-kinase inhibitor H1152, using a filter based fractionation method.
Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against estrogen receptor alpha (ESR1). Gene expresion of estrogen receptor alpha (ESR1) was knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with non-targetting control treated cells were analysed using Affymetrix Human Genome U133 Plus 2.0 microarrays.
Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against 78 transcription factors and signalling molecules. Gene expresion of 78 functionally important molecules were knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with untreated cells and non-targetting control (SICONTROL) treated cells were analysed using microarrays.
Project description:To knock down SLC3A2, MCF10A cells were either transfected with control siRNAs, or siRNAs specifically targetting SLC3A2. Samples were either untreated or treated with TGFb. Ribosome profiling and RNA sequencing was performed on these samples. MCF10A cells with and without SLC3A2 overexpression construct were either untreated or treated with TGFb. Ribosome profiling was performed on these samples.