827a61e7-cbae-480f-9c80-fa8aa104f4c6 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001011137 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:This dataset gather HiChIP data for H3K27ac mar in MM.1S cell line in control and Dex condition, both in two biological replicates
| EGAD00001011138 | EGA
Project description:This dataset gather scMultiomic data including RNA-seq and ATAC-seq in MM.1S in control and dex condition at 1h and 4h
| EGAD00001011140 | EGA
Project description:This dataset gather scRNAseq data performed for MM.1S cell line in control and dex conditions at 4h and 24h
| EGAD00001011139 | EGA
Project description:This dataset gather ChIP-seq data produced by immunoprecipitating CTCF factor in own laboratory in MM.1S cell line in EtOH and Dex conditions. It also gather ChIP-seq dataset produced by external laboratory (Active Motif) for H3K27ac mark and GR transcription factor in same cell line and conditions ( MM.1S ETOH/Dex)
| EGAD00001011136 | EGA
Project description:This dataset contains ATAC-seq data performed in MM.1S cell line in ETOH (control) or Dexamethasone condition (Treatment)
| EGAD00001011135 | EGA
Project description:We previously noted that combination glucocorticoids and PI3K inhibition induces synergistic cell death. To identify genes involved in myeloma cell death we examined mRNA expression in each individual treatment and in the combination. The glucocoriticoid resistant cells (MM.1RL) are used as a negative control. Gene expression is assessed using Illumina Human HT-12v4 bead chips For this experiment, the lab is using human multiple myeloma cell lines that were isolated from a patient. MM.1S cells display sensitivity to glucocorticoids. MM.1RL cells display resistance to glucocorticoid treatment due to spontaneous mutations that render the glucocorticoid receptor inoperable. In this experiment, there will be 4 conditions for the MM.1S cells, and 2 conditions for the MM.1RL cells. We will be treating the MM.1S cells with a glucocorticoid alone (Dexamethasone - 1 uM), a PI3K inhibitor alone (LY249002 - 25 uM), a combination of the two drugs, and a vehicle control. The MM.1RL cells will be treated with a PI3K inhibitor alone, and with a vehicle control. Since the PI3K inhibitor is diluted in DMSO, as a control an equal volume of DMSO will be added to all conditions not containing the PI3K inhibitor. Conditions within the MM.1S cell line will be compared with each other. Specifically, we hope to identify genes that are similarly affected by all three experimental conditions. The MM.1RL conditions will not be analyzed at this time. There will be 4 biological replicates of each condition.
2015-12-07 | E-GEOD-64704 | biostudies-arrayexpress
Project description:The transcriptional profile of the human multiple myeloma (MM) cell line MM.1S treated with MLN4924 vs control MM.1S cells was characterized by oligonucleotide microarray analysis, using the human U133 plus 2.0 Affymetrix GeneChip, according to previously described protocols for total RNA extraction and purification; cDNA synthesis; in vitro transcription reaction for production of biotin-labeled cRNA; hybridization of cRNA with U133plus2.0 Affymetrix gene chips; and scanning of image output files. Scanned image output files were analyzed using DNA-Chip Analyzer (dChip) (www.dchip.org), including conversion to DCP files, normalization and modeling. The gene expression profile of MM.1S cells for each time point of MLN4924 treatment was compared to the profile of control MM.1S cells. The NEDD8 activating enzyme (NAE) is upstream of the 20S proteasome in the ubiquitin/proteasome pathway and catalyzes the first step in the neddylation pathway. NEDD8 modification of cullins is required for ubiquitination of cullin-ring ligases (CRLs), which regulate degradation of a distinct subset of proteins. The more targeted impact of NAE on protein degradation prompted us to study MLN4924, an investigational NAE inhibitor, in preclinical multiple myeloma (MM) models. In vitro treatment with MLN4924 led to dose-dependent decrease of viability in a panel of human MM cell lines. In this analysis, we evaluated the molecular changes triggered in MM.1S myeloma cells by their in vitro treatment with MLN4924. The transcriptional profiles of each experimental condition were characterized by oligonucleotide microarray analysis, using the human U133 plus 2.0 Affymetrix GeneChip.
2012-05-02 | GSE33577 | GEO
Project description:Purpose: We report the NGS-derived transcriptome profiling (paired-end RNA-seq) following proteasome inhibition in the multiple myeloma cell line MM.1S. Methods: MM.1S cells were treated for six hours with the synthetic proteasome inhibitor lactacystin and RNA expression changes were quantified and compared to DMSO control-treated cells by RNA-sequencing.
2022-11-21 | GSE193300 | GEO
Project description:Purpose: We report the NGS-derived transcriptome profiling (paired-end RNA-seq) following proteasome inhibition in the multiple myeloma cell line MM.1S. Methods: MM.1S cells were treated for six hours with the synthetic proteasome inhibitor lactacystin or clinically-approved proteasome inhibitor bortezomib and RNA expression changes were quantified and compared to DMSO control-treated cells by RNA-sequencing.
2021-03-06 | GSE166122 | GEO
Project description:Multiple myeloma (MM) evolves from highly prevalent premalignant condition termed Monoclonal Gammopathy of Undetermined Significance (MGUS). We report an MGUS-MM phenotype arising in transgenic mice with Emu-directed expression of the unfolded protein/ER stress response and plasma cell development spliced isoform factor XBP-1s. Emu-XBP-1s elicited elevated serum Ig and IL-6 levels, skin alterations and with advancing age, a significant proportion of Emu-xbp-1s transgenic mice develop features diagnostic of human MM including bone lytic lesions. Transcriptional profiles of Emu-xbp-1s B lymphoid and MM cells show aberrant expression of genes known to be dysregulated in human MM including Cyclin D1, MAF, MAFB, and APRIL. This genetic model coupled with documented frequent XBP-1s overexpression in human MM serve to implicate chronic XBP-1s dysregulation in the development of this common and lethal malignancy. Keywords: XBP-1, MGUS, multiple myeloma, transgenic mouse
2007-04-09 | GSE6980 | GEO