Project description:Sicyoidochytrium minutum DNA virus strain 001 (SmDNAV 001) is a double-stranded DNA (dsDNA) virus that infects the marine fungoid protist Sicyoidochytrium minutum. We report the draft genome sequence of SmDNAV 001. The 236,345-bp genome contained 358 coding sequences (CDSs) and 3 tRNA-coding sequences.
Project description:We examined the effects of ICG-001 on gene expression in Mel202 uveal melanoma (UM) cells. ICG-001 exerted strong antiproliferative activity against UM cells, leading to cell cycle arrest, apoptosis, and inhibition of migration. Global gene expression profiling revealed strong suppression of genes associated with cell cycle proliferation, DNA replication, and G1/S transition. Gene set enrichment analysis revealed that ICG-001 suppressed Wnt, mTOR, and MAPK signaling. Strikingly, ICG-001 suppressed the expression of genes associated with UM aggressiveness, including CDH1, CITED1, EMP1, EMP3, SDCBP, and SPARC. Notably, the transcriptomic footprint of ICG-001, when applied to a UM patient dataset, was associated with better clinical outcome. Lastly, ICG-001 exerted anticancer activity against a UM tumor xenograft in mice.
Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays
Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin)
Project description:Purpose: The goal of this study was to investigate the TLR9 specific immune effects of anti-Qbeta-coated CMP-001 using the following groups: untreated, anti-Qbeta coated CMP-001, anti-Qbeta coated CMP-001 with methylated and thus, inactive ODN (mCMP-001), and G10 (naked TLR9 agonist). Methods: Unfractionated PBMCs from a healthy donor were isolated via ficol gradient and treated with and without anti-Qbeta coated CMP-001 (10ug/ml), anti-Qbeta coated mCMP-001 (inactive ODN; 10ug/ml), or G10 (naked TLR9 agonist; 2.5ug/ml) for 24 hours. Untreated and treated fractions were sequenced on an Illumina NovaSeq 6000 system. FASTQ files were generated from basecall files with the bcl2fastq software (Illumina) provided by the University of Iowa Institute of Human Genetics. Data files were subsequently downloaded to Argon and mapped to the prebuilt GRCh38 genome with CellRanger (version 3.0.1). After initial mapping datasets were merged together and clustering was performed based on merged data sets using Cell Ranger software. Cells with unique gene counts fewer than 300 or more than 4,000 per cell were eliminated along with a mitochondria gene cutoff of 25%. Log normalization of aggregated reads was performed with Seurat (version 3.0.2) using a scale factor of 10,000. Feature selection was performed with the variance stabilizing transformation before integration was performed with Seurat (v3.0.1). Results: A total of 17,280 cells were recovered after filtering. Clusters were identified based on expression of unique gene markers. Differential expression analysis identified genes enriched in each populatin of cells corresponding to untreated versus treated libraries. Particular empasis was given to genes enriched in monocytes. Conclusions: We report that CMP-001 induces a variety of immune responses in each cell cluster, with a unique gene signature displayed by monocytes.