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

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

PROVIDER: PRJNA874034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21231527_1.fastq.gz	Fastqsanger.gz
	SRR21231527_2.fastq.gz	Fastqsanger.gz
	SRR21231528_1.fastq.gz	Fastqsanger.gz
	SRR21231528_2.fastq.gz	Fastqsanger.gz
	SRR21231529_1.fastq.gz	Fastqsanger.gz

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Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-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 | GSE212108 | GEO

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

2023-04-23 | GSE212107 | GEO

Lamin B1 overexpression alters chromatin organization and gene expression

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

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

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

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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

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Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity

Project description:The nuclear lamins are extremely long-lived proteins in most cell types. As a consequence, lamin function cannot be effectively dissected with temporal precision using standard knock-down approaches. Here, we apply the auxin inducible degron (AID) system to rapidly deplete each lamin isoform within one cell cycle and reveal the immediate impacts of lamin loss on the nucleus . Surprisingly, neither acute lamin A/C (LA/C), lamin B1 (LB1), nor lamin B2 (LB2) depletion altered nuclear shape or induced nuclear blebbing, indicating that acute lamin loss is not sufficient to alter nuclear morphology. LB1 depletion is immediately followed by LA/C meshwork disorganization due to actin cytoskeletal forces on the lamina, yet neither LA/C nor LB1 depletion induced nuclear rupturing. We found that the abundant inner nuclear membrane protein LAP2β protects nuclear integrity in the absence of LB1, as depletion of both LB1 and LAP2β induced severe LA/C disorganization and frequent nuclear rupturing. Depolymerization of the actin cytoskeleton halts nuclear rupture in LAP2β- and LB1-depleted nuclei. We conclude that both LB1 and LAP2β resist cytoskeletal force to maintain regular lamin A/C meshwork organization and preserve nuclear integrity.

2025-02-17 | GSE289252 | GEO

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

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