Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lamin B1 overexpression alters chromatin organization and gene expression (mRNA-seq)

ABSTRACT: Lamin B1 overexpression alters chromatin organization and gene expression (mRNA-seq)

PROVIDER: PRJNA874035 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21232723_1.fastq.gz	Fastqsanger.gz
	SRR21232723_2.fastq.gz	Fastqsanger.gz
	SRR21232724_1.fastq.gz	Fastqsanger.gz
	SRR21232724_2.fastq.gz	Fastqsanger.gz
	SRR21232725_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Lamin B1 overexpression alters chromatin organization and gene expression

Project description:Lamin B1 overexpression alters chromatin organization and gene expression

| PRJNA874026 | ENA

Lamin B1 overexpression alters chromatin organization and gene expression (mRNA-seq)

Project description:Overexpression of Lamin B1 leads to the redistribution of H3K9me3 heterochromatin away from the nuclear periphery and into heterochromatic DNA foci within the nucleoplasm. These changes in chromatin organization correlate with misregulated gene expression (mRNA-sequencing), but do not correlate with altered H3K9me3 deposition across the genome (Cut&Run).

2023-04-23 | GSE212107 | GEO

Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-seq)

2023-04-23 | GSE212108 | GEO

Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-seq)

Project description:Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-seq)

| PRJNA874034 | ENA

Lamin B1 ChIPseq experiments from ER:RAS IMR90s

Project description:Lamin B1 from OIS IMR90s We used ChIP-seq to examine the global binding of Lamin B1 in human IMR90 oncogene-induced senescence

2014-12-15 | E-GEOD-53331 | biostudies-arrayexpress

Lamin B1 overexpression alters chromatin organization and gene expression.

Project description:Peripheral heterochromatin positioning depends on nuclear envelope associated proteins and repressive histone modifications. Here we show that overexpression (OE) of Lamin B1 (LmnB1) leads to the redistribution of peripheral heterochromatin into heterochromatic foci within the nucleoplasm. These changes represent a perturbation of heterochromatin binding at the nuclear periphery (NP) through a mechanism independent from altering other heterochromatin anchors or histone post-translational modifications. We further show that LmnB1 OE alters gene expression. These changes do not correlate with different levels of H3K9me3, but a significant number of the misregulated genes were likely mislocalized away from the NP upon LmnB1 OE. We also observed an enrichment of developmental processes amongst the upregulated genes. ~74% of these genes were normally repressed in our cell type, suggesting that LmnB1 OE promotes gene de-repression. This demonstrates a broader consequence of LmnB1 OE on cell fate, and highlights the importance of maintaining proper levels of LmnB1.

| S-EPMC10114975 | biostudies-literature

Lamin B1 dependent transcriptional control in neural progenitor cells

Project description:Through knocking out Lamin B1, we found that lamin B1 regulets hundreds of genes in neural progenitor cells, which underlie differentiation of neural protenitor cells

2021-02-10 | GSE156156 | GEO

Lamin B1 ChIPseq experiments from ER:RAS IMR90s

Project description:Lamin B1 from OIS IMR90s

2014-12-15 | GSE53331 | GEO

Human lamin B1: stress-induced phosphorylation

Project description:This is a small scale study of the phosphorylation state of human lamin B1 immunoprecipitated from control cells or cells treated with methyl methane sulphonate (MMS, acting as a DNA damage stressor agent)

2017-05-30 | PXD006459 | Pride

Lamin B1 regulates somatic mutations and progression of B cell malignancies

Project description:Somatic hypermutation (SHM) is a pivotal process in adaptive immunity that occurs in the germinal centre and allows B-cells to change their primary DNA sequence and diversify their antigen receptors. Here, we report that genome binding of Lamin B1, a component of the nuclear envelope involved in epigenetic chromatin regulation, is reduced during B cell activation and formation of lymphoid germinal centres. ChIP-Seq analysis showed that kappa and heavy variable immunoglobulin domains were released from the Lamin B1 suppressive environment when SHM was induced in B cells. RNAi-mediated reduction of Lamin B1 resulted in spontaneous SHM as well as kappa-light chain aberrant surface expression. Finally, Lamin B1 expression level was directly proportional to 5-year survival rate in chronic lymphocytic leukaemia, and was strongly involved in transformation of follicular lymphoma. In summary, here we report that Lamin B1 is a negative epigenetic regulator of SHM in normal B-cells and a "mutational gatekeeper", suppressing the aberrant mutations that drive lymphoid malignancy.

2017-08-03 | GSE89869 | 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