Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Relief of extracellular matrix deposition repression by downregulation of IRF1-mediated TWEAK/Fn14 signaling in keloids

ABSTRACT: Relief of extracellular matrix deposition repression by downregulation of IRF1-mediated TWEAK/Fn14 signaling in keloids

PROVIDER: PRJNA914216 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22826517_1.fastq.gz	Fastqsanger.gz
	SRR22826517_2.fastq.gz	Fastqsanger.gz
	SRR22826518_1.fastq.gz	Fastqsanger.gz
	SRR22826518_2.fastq.gz	Fastqsanger.gz
	SRR22826519_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Relief of extracellular matrix deposition repression by downregulation of IRF1-mediated TWEAK/Fn14 signaling in keloids

Project description:Keloids represent a fibrotic disorder characterized by the excessive deposition of extracellular matrix (ECM). However, the mechanisms by which ECM deposition in keloids is regulated remain elusive. Here, we found that the expression of both TWEAK and its cognate receptor Fn14 was significantly downregulated in keloids and that TWEAK/Fn14 signaling repressed the expression of ECM-related genes in keloid fibroblasts. The IRF1 gene was essential for this repression, and the TWEAK/Fn14 downstream transcription factor P65 directly bound to the promoter of the IRF1 gene and induced its expression. Furthermore, in keloid patients, the expression of TWEAK and Fn14 was negatively correlated with that of ECM genes and positively correlated with that of IRF1. These observations indicate that relief of TWEAK/Fn14/IRF1-mediated ECM deposition repression contributes to keloid pathogenesis, and the identified mechanism and related molecules provide potential targets for keloid treatment in the future.

2023-01-28 | GSE221382 | GEO

TMT-coupled phosphoproteomics support novel role of TWEAK/Fn14 signaling in synaptic function

Project description:The study aims at illustrate novel role of TWEAK/Fn14 signaling in synapse function by combining electrophysiological and phosphoproteomic approaches. The results show that TWEAK acutely dampens basal synaptic transmission and plasticity through neuronal Fn14 and impacts the phosphorylation state of pre- and post-synaptic proteins in adult mouse hippocampal slices. Two models featuring synaptic deficits were used in the study. Blocking TWEAK/Fn14 signaling augments synaptic function in hippocampal slices from amyloid beta-overexpressing mice. After stroke, genetic or pharmacological inhibition of TWEAK/Fn14 signaling augments basal synaptic transmission and normalizes plasticity. Our data support a glial/neuronal axis that critically modifies synaptic physiology and pathophysiology in different contexts in the mature brain and may be a therapeutic target for improving neurophysiological outcomes.

2021-02-02 | PXD021582 | Pride

TWEAK/Fn14 signalling in Breast Cancer [p52_ChIP]