Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ChIP-seq]

ABSTRACT: ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ChIP-seq]

PROVIDER: PRJNA678324 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13057296_1.fastq.gz	Fastqsanger.gz
	SRR13057296_2.fastq.gz	Fastqsanger.gz
	SRR13057297_1.fastq.gz	Fastqsanger.gz
	SRR13057297_2.fastq.gz	Fastqsanger.gz
	SRR13057298_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation

Project description:ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation

| PRJNA678329 | ENA

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ATAC-seq]

Project description:ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ATAC-seq]

| PRJNA678314 | ENA

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ChIP-seq]

Project description:Matrix stiffness is a central regulator of fibroblast function. However, the transcriptional mechanisms linking matrix stiffness to changes in fibroblast phenotype are incompletely understood. Here, we evaluated the effect of matrix stiffness on genome-wide chromatin accessibility in freshly-isolated lung fibroblasts using ATAC-seq. We found higher matrix stiffness profoundly increased global chromatin accessibility relative to lower matrix stiffness, and these alterations were in close genomic proximity to known pro-fibrotic gene programs. Motif analysis of these regulated genomic loci identified ZNF416 as a putative mediator of fibroblast stiffness responses. Genome occupancy analysis using ChIP-seq confirmed that ZNF416 occupies a broad range of genes implicated in fibroblast activation and tissue-fibrosis, with relatively little overlap in genomic occupancy with other mechanoresponsive and pro-fibrotic transcriptional regulators. Using loss and gain of function studies we demonstrated that ZNF416 plays a critical role in fibroblast proliferation, extracellular matrix synthesis and contractile function. Together these observations identify ZNF416 as novel mechano-activated transcriptional regulator of fibroblast biology.

2020-11-14 | GSE161446 | GEO

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation [ATAC-seq]

2020-11-14 | GSE161434 | GEO

ZNF416 is a pivotal transcriptional regulator of fibroblast mechano-activation

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

2020-11-14 | GSE161448 | GEO

An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

Project description:An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

| PRJNA1118198 | ENA

An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

Project description:An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

| PRJNA1154956 | ENA

TEAD1 in cardiac fibroblast activation

Project description:TEAD1 in cardiac fibroblast activation

| PRJNA1064074 | ENA

An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

Project description:Nature creates specific structures to control mechanical plasticity for cell fate regulation. Although immune cells can sense and adapt to extracellular mechanical cues, how to activate immune responses via intracellular mechanical stimulation remains a mystery. Here, we present an intelligent intracellular magnetic torque (IIMT) paradigm that is coupled with programmed rotating magnetic fields to generate the selective mechano-stimulations in lysosomes and induce sequential antitumor immune responses. A magnetic rod-shaped micromotor (MagRM) with the a unique geometric aspect ratio is designed to exert tunable torques in antigen-presenting cells (APCs) and tumor cells. Low-intensity torque induces the mild lysosomal membrane damage to trigger antigen cross-presentation and canonical NLRP3 inflammasome activation in APCs, whereas high-intensity torque causes lysosomal membrane rupture for immunogenic cell death. In vivo studies unveil that the optimal antitumor activity is achieved by generating sequential torques from high to low intensities, which is illuminating to explore mechano-immunotherapy with selective and spatiotemporal control.

2025-10-15 | GSE268655 | GEO

An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

2025-10-15 | GSE276125 | GEO