Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq and RNA-seq analyses in human multiple myeloma cell line MM.1S

ABSTRACT: ChIP-seq and RNA-seq analyses in human multiple myeloma cell line MM.1S

PROVIDER: PRJNA622952 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11476868.fastq.gz	Fastqsanger.gz
	SRR11476869.fastq.gz	Fastqsanger.gz
	SRR11476870.fastq.gz	Fastqsanger.gz
	SRR11476871.fastq.gz	Fastqsanger.gz
	SRR11476872.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

Transcription profiling of human U266, MM.1s, KMS11, 8226/S multiple myeloma cell lines treated with arsenic

Project description:We used microarrays to examine changes in gene expression in multiple myeloma cell lines following treatment with arsenic trioxide and darinaparsin Experiment Overall Design: Four multiple myeloma cell lines (U266, MM.1s, KMS11, 8226/S) were treated with either arsenic trioxide (ATO) for 6, 24, or 48 hours or darinaparsin (DAR) for 6 or 24 hours; RNA was extracted from treated and control cells for microarray analysis

2009-02-01 | E-GEOD-14519 | biostudies-arrayexpress

Global proteomics in MM.1S treated with pomalidomide or dipeptides

Project description:Global proteomics of Multiple Myeloma cell line MM.1S treated with pomalidomide or cyclic imide dipeptides for 10 h. The samples were labeled with TMT-16pro.

2022-07-28 | PXD025336 | Pride

Multiple Myeloma cells

Project description:Multiple Myeloma cell line MM.1S performed ChIP-seq analysis using anti-c-Fos antibody.

2022-01-30 | GSE194381 | GEO

RNA-seq analysis after JQKD82 treatment in human multiple myeloma cell line MM.1S

Project description:RNA-seq analysis after JQKD82 treatment in human multiple myeloma cell line MM.1S

| PRJNA622959 | ENA

ChIP-seq and RNA-seq analyses in human multiple myeloma cell line MM.1S

Project description:Recent studies have highlighted the oncogenic roles of KDM5A; however, its molecular mechanism has not been fully delineated. Here we identifies KDM5A as a transcriptional activator of MYC target genes in multiple myeloma (MM). Genetic ablation of KDM5A or pharmacologic inhibition of KDM5 by novel inhibitor JQKD82 impairs MM cell growth. Gene expression profile reveals that JQKD82 decreases expression of MYC targets. Expression of MYC targets is similarly downregulated by KDM5A depletion, but little affected by KDM5B knockdown. Mechanistically, KDM5A co-localizes with MYC across the genome, and KDM5A and MYC coordinately promote MYC target gene transcription. The treatment with JQKD82 reduces phosphorylation level of RNA polymerase II (RNAPII), resulting in RNAPII pausing, accompanied by hyper-H3K4me3 status at the MYC loci. Finally, we shows that JQKD82 exerts anti-MM activity and prolongs overall survival in vivo mouse xenograft models. Our results delineate KDM5A function that reinforces MYC transcriptional program, and identify KDM5A as a potential therapeutic target in MM. This SuperSeries is composed of the SubSeries listed below.

2021-03-22 | GSE148048 | GEO

Transcription profiling of mouse multiple myeloma tumors and splenic B cells from transgenics overexpressing XBP-1s

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. Experiment Overall Design: In this study, we have explored the biological impact of sustained XBP-1s expression in the lymphoid system, anticipating that this genetic event would be a necessary component along with other MM-relevant oncogenes and tumor suppressor gene manipulations to generate a MM-prone mouse model. Unexpectedly, XBP-1s overexpression alone yielded an MGUS-MM disease bearing many features classical of the human disease on the clinical, pathological and molecular levels. Experiment Overall Design: We performed expression analysis of B cells derived from the spleen of 20-week old Emu-xbp-1s mice (n=5) and non-transgenic mice (n=5). Additionally, we analyzed the expression profiles from MM tumor cells arising in Emu-xbp-1s mice (n=6).

2007-11-06 | E-GEOD-6980 | biostudies-arrayexpress

ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

Project description:ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

| PRJNA622960 | ENA

ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

2021-03-22 | GSE148046 | GEO

The Differentiation and Stress Response Factor, XBP-1, Drives Multiple Myeloma Pathogenesis

2007-04-09 | GSE6980 | GEO

The mitochondrial protease LonP1 promotes proteasome inhibitor resistance in multiple myeloma.

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data