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Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria

ABSTRACT: Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria

PROVIDER: PRJNA450863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10597460.fastq.gz	Fastqsanger.gz
	SRR10597461.fastq.gz	Fastqsanger.gz
	SRR10597462.fastq.gz	Fastqsanger.gz
	SRR10597463.fastq.gz	Fastqsanger.gz
	SRR10597464.fastq.gz	Fastqsanger.gz

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Similar Datasets

GRO-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. In progeria-patient fibroblasts, a subset of pS22-Lamin A/C-binding sites were lost whereas new pS22-Lamin A/C-binding sites emerged in normally quiescent loci. New pS22-Lamin A/C binding was accompanied by increased histone acetylation, increased c-Jun binding, and upregulation of nearby genes implicated in progeria pathophysiology. These results suggest that Lamin A/C regulates gene expression by enhancer binding. Disruption of the gene regulatory rather than LAD tethering function of Lamin A/C presents a novel mechanism for disorders caused by LMNA mutations.

2020-02-15 | GSE113350 | GEO

RNA-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

2020-02-15 | GSE113343 | GEO

ChIP-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

2020-02-15 | GSE113291 | GEO

ATAC-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

2020-02-15 | GSE113352 | GEO

ChIP-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:ChIP-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

| PRJNA450847 | ENA

RNA-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:RNA-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

| PRJNA450854 | ENA

ATAC-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:ATAC-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

| PRJNA450862 | ENA

GRO-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:GRO-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

| PRJNA450859 | ENA

Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-02-15 | GSE113354 | GEO

Single-Dose CRISPR/Cas9 Therapy Extends Lifespan of Mice with Hutchinson-Gilford Progeria Syndrome

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare lethal genetic disorder characterized with symptoms reminiscent of accelerated aging. The major underlying genetic cause is a substitution mutation in the gene coding for lamin A, causing the production of a toxic isoform called progerin. Here we show the RNA sequencing analyses performed on primary mouse fibroblasts of different genotypes (in terms of Progeria; Cas9 background) treated with Cas9 guide RNAs targeting Lmna/Progerin. The mouse genetic background in (1) Pro/Pro;Cas9/+: homozygous for Progeria and heterozygous for transgenic Cas9 The mouse genetic background in (2) Pro/+; +/+: heterozygous for Progeria and no transgenic Cas9 (wild type) The mouse genetic background in (3) +/+;Cas9/+: no Progeria (wild type) and heterozygous for transgenic Cas9

2019-02-15 | GSE122865 | GEO

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