Escherichia coli strain:TOK-001
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REPOSITORIES: ENA
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Project description:UFH-001 cells, a newly isolated breast cancer line, have an STR profile that is most similar to that of the control MCF10A cells. Yet, the UFH-001 line is tumor forming with a triple negative phenotype. These cells have a unique transcriptome profile associated numerous breast cancer marker genes. We used microarrays to detail the global programme of gene expression underlying the metastatic behavior of the UFH-001 cells compared to the MCF10A cells.
2018-06-01 | GSE107209 | GEO
Project description:Escherichia coli 93-001 genome sequencing project
| PRJNA65775 | ENA
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.
2020-04-28 | GSE149417 | GEO
Project description:Escherichia coli strain:ZJJY | isolate:001 Genome sequencing
| PRJNA1026160 | ENA
Project description:Radiation provides excellent tumor control in prostate cancer yet unavoidably harms adjacent healthy tissue via the generation of reactive oxygen species (ROS). Radiation-induced ROS is known to impact fibroblasts long after radiation, resulting in radiation-induced fibrosis (RIF), which can cause incontinence and other side effects that reduce patient quality of life. BMX-001, a manganese porphyrin designed to mimic superoxide dismutase, is in clinical trials as a selective radioprotector when given before and during radiation therapy. However, there have been no studies evaluating BMX-001 when given after radiation for its impacts on RIF. Mice were given pelvic radiation (7.5 Gy for 5 consecutive days) followed by BMX-001 three weeks after radiation. Fibroblasts and tissues were isolated two months following radiation. We found that BMX-001 returned radiation-induced alterations in fibroblast morphology to normal and reversed markers of fibroblast activation and senescence. BMX-001 also decreased collagen deposition six months after radiation. We found that overall, radiation resulted in reduced methylation two months after radiation, and BMX-001 administered three weeks after radiation modulated radiation-altered methylation patterns back to normal and restored normal expression of a fibrosis-associated gene CAMK2beta. BMX-001 also decreased radiation-induced DNA adduct 8-hydroxy-2’-deoxyguanosine (8-OHdG), which is known to interfere with methylation. BMX-001 was able to prevent DNA oxidation and restore normal methylation patterns in an oligonucleotide model of DNA oxidation and methylation. This study reveals the feasibility of agents to reverse fibrosis in pelvic radiation and suggests that BMX-001 may be effective when given after radiation.
2026-01-28 | GSE308163 | GEO
Project description:Radiation provides excellent tumor control in prostate cancer yet unavoidably harms adjacent healthy tissue via the generation of reactive oxygen species (ROS). Radiation-induced ROS is known to impact fibroblasts long after radiation, resulting in radiation-induced fibrosis (RIF), which can cause incontinence and other side effects that reduce patient quality of life. BMX-001, a manganese porphyrin designed to mimic superoxide dismutase, is in clinical trials as a selective radioprotector when given before and during radiation therapy. However, there have been no studies evaluating BMX-001 when given after radiation for its impacts on RIF. Mice were given pelvic radiation (7.5 Gy for 5 consecutive days) followed by BMX-001 three weeks after radiation. Fibroblasts and tissues were isolated two months following radiation. We found that BMX-001 returned radiation-induced alterations in fibroblast morphology to normal and reversed markers of fibroblast activation and senescence. BMX-001 also decreased collagen deposition six months after radiation. We found that overall, radiation resulted in reduced methylation two months after radiation, and BMX-001 administered three weeks after radiation modulated radiation-altered methylation patterns back to normal and restored normal expression of a fibrosis-associated gene CAMK2beta. BMX-001 also decreased radiation-induced DNA adduct 8-hydroxy-2’-deoxyguanosine (8-OHdG), which is known to interfere with methylation. BMX-001 was able to prevent DNA oxidation and restore normal methylation patterns in an oligonucleotide model of DNA oxidation and methylation. This study reveals the feasibility of agents to reverse fibrosis in pelvic radiation and suggests that BMX-001 may be effective when given after radiation.
2026-01-28 | GSE309064 | GEO
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.
2021-06-30 | GSE172493 | GEO
Project description:Proteus mirabilis AOUC-001 complete genome
| PRJNA318385 | ENA
Project description:Fusarium sp. GX-001 mitochondrion, complete genome
| PRJNA780977 | ENA
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)
2014-07-15 | GSE57728 | GEO