Project description:4-Hydroxynonenal (HNE), a cytotoxic and diffusible electrophile generated by the spontaneous decomposition of oxidized lipids, has a suspected role in neurodegenerative and inflammatory disease processes. In addition to promoting cell death, elevated levels of HNE lead to the engagement of cytoprotective signaling pathways, including the heat shock, antioxidant, DNA damage, and ER stress responses. Activation of the heat shock response, mediated by the transcription factor heat shock factor 1 (HSF1), is critical for maintaining cellular viability in the presence of HNE. Accordingly, silencing HSF1 expression using siRNA enhances the toxicity of HNE. Microarray analysis of samples from control and HSF1-silenced cells was performed to investigate which associated changes in gene could be responsible for the decrease in cellular viability. Four different experimental conditions were investigated. Samples were prepared and analyzed in triplicate. Samples 1-3 received NEG control siRNA and DMSO (vehicle) for 6 h. Samples 4-6 received NEG control siRNA and 50 uM HNE for 6 h. Samples 7-9 received HSF1 siRNA and DMSO (vehicle) for 6 h. Samples 10-12 received HSF1 siRNA and 50 uM HNE for 6 h.
Project description:4-Hydroxynonenal (HNE), a cytotoxic and diffusible electrophile generated by the spontaneous decomposition of oxidized lipids, has a suspected role in neurodegenerative and inflammatory disease processes. In addition to promoting cell death, elevated levels of HNE lead to the engagement of cytoprotective signaling pathways, including the heat shock, antioxidant, DNA damage, and ER stress responses. Activation of the heat shock response, mediated by the transcription factor heat shock factor 1 (HSF1), is critical for maintaining cellular viability in the presence of HNE. Accordingly, silencing HSF1 expression using siRNA enhances the toxicity of HNE. Microarray analysis of samples from control and HSF1-silenced cells was performed to investigate which associated changes in gene could be responsible for the decrease in cellular viability.
Project description:The objective of this experiment was to compare the transcriptional profile of TBBR (TGFbRII ectodomain fused to 41BB endodomain) vs control ΔTGFbRII (truncated version that lacks an endodomain) modified T cells. RNA samples were isolated from trangenic T cells generated from three independent donors.
Project description:We analyzed the total proteome of CD4+ T cells isolated from WT mice, and cultured to perform a CRISPR/CAS9 edition of their genome, in order to introduce an OST sequence at the C-terminus of proteins of interest (LAT or UBASH3A, n=6 biological replicates in each case). Control CD4+ T cells , isolated and cultured in the same way, but not modified by CRISPR/CAS9, were also analyzed (CT, n=6 biological replicates), as well as CD4+ T cells which have undergone a smaller number of expansion cycles than long term CD4+ T cells (WT, n=2 biological replicates). Each sample was analyzed once by single run naoLC-MS, resulting in 20 raw files.
Project description:The objective of this experiment was to compare the transcriptional profile of 4/7 ICR (IL4R ectodomain fused to IL7R endodomain) vs control ΔIL4R (truncated version that lacks an endodomain) modified T cells. RNA samples were isolated from trangenic T cells generated from three independent donors.
Project description:Observational, Multicenter, Post-market, Minimal risk, Prospective data collection of PillCam SB3 videos (including PillCam reports) and raw data files and optional collection of Eneteroscopy reports
Project description:Temporal analysis of Irf4 and PU.1 genome binding during B cell activation and differentiation in vitro using antigen (NP-Ficoll) CD40L and IL-2/4/5 cytokines (see Molecular Systems Biology 7:495 for details of cellular system). The results provide insight in the target genes and binding specificity of IRF4 and PU.1 during coordination of different programs of B cell differentiation. Regrettably three of the FASTQ raw sequence files in our study were corrupted during storage. FASTQ data from our experimental and control groups are available for download via GEO SRA; however, two groups are missing select raw sequence files. These include one PU.1 Day 3 group file (Sample GSM1133499) and two of four input files used to generate a concatenated “super” input file (Sample GSM1133490); the raw data provided for input consists of the two input files recovered. Importantly, FASTA sequences for both of these datasets are available as supplementary data through GEO, and we can make available upon request (rsciamma@uchicago.edu) all files in our study in the ELAND-extended alignment format. Please note that GEO no longer supports this format.
Project description:We observed gene expression difference between different groups after MDA-MB-231 treated with DMSO, 10 μM DAC, 1 μM DEX, or DAC+DEX. Data obtained from high-throughput sequencing (Illumina NovaSeq 6000 platform) were transformed into raw sequenced reads by CASAVA base calling and stored in FASTQ format. Gene expression of each groups are listed in raw data files. Some different expression genes between two groups are further validated with qRT-PCR.
Project description:The objective of this experiment was to compare the transcriptional profile of T cells modified to express CAR, TBBR and 4/7 ICR (i.e. SmarT-cells) against control T cells expressing the delta constructs (i.e. ΔCAR, ΔTGFbRII and ΔIL4R). RNA samples were isolated from trangenic T cells generated from three independent donors.