Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [mouse_ASC]

ABSTRACT: Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [mouse_ASC]

PROVIDER: PRJNA1028297 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26388239_1.fastq.gz	Fastqsanger.gz
	SRR26388239_2.fastq.gz	Fastqsanger.gz
	SRR26388240_1.fastq.gz	Fastqsanger.gz
	SRR26388240_2.fastq.gz	Fastqsanger.gz
	SRR26388241_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [mouse_ASC]

Project description:Purpose: TGF-β/BMP signaling pathway has a significant role in fibrotic cataract. Smurf1, a ubiquitin protein ligase, regulates the TGF-β/BMP signaling pathway through the ubiquitin-proteasome system (UPS). This study aims to investigate the role of Smurf1 in the progression of fibrotic cataract and its underlying mechanism.Method: We employed a mouse injury-induced anterior subcapsular cataract (ASC) model and administered Smurf1 inhibitor A01 through anterior chamber injection for in vivo investigation. RNA sequencing was performed to examine global gene expression changes. The volume of the subcapsular opacity was determined using whole-mount immunofluorescence of lens anterior capsules. Lentivirus was utilized to create cell lines with Smurf1 knockdown or overexpression in SRA01/04. Protein levels were assessed by Simple Western. Lens epithelial cell (LEC) proliferation was evaluated by CCK8 and EdU assays. LEC migration was measured by Transwell and wound healing assays.Results: The mRNA levels of genes associated with cell proliferation, migration, epithelial-mesenchymal transition (EMT), TGF-β/BMP pathway and UPS, including Smurf1, were upregulated in ASC model. The mRNA expression of Smurf1 was also upregulated in anterior lens capsules of age-related cataract patients. Anterior chamber injection of A01 inhibited ASC formation and EMT. In vitro knockdown of Smurf1 resulted in reduced proliferation, TGF-β2-induced migration and EMT of LECs. Smurf1 inhibition upregulated Smad1, Smad5 and pSmad1/5. Conversely, Smurf1 overexpression displayed the opposite phenotypes.Conclusion: Smurf1 regulated the progression of fibrotic cataract by influencing the proliferation, migration and EMT of LECs through regulation of Smad signaling pathway, offering a novel target for the treatment of fibrotic cataract.

2024-02-14 | GSE245411 | GEO

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [cell line]

2024-02-14 | GSE245407 | GEO

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation

Project description:Smurf1 modulates Smad signaling pathway in fibrotic cataract formation

| PRJNA1028296 | ENA

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [cell line]

Project description:Smurf1 modulates Smad signaling pathway in fibrotic cataract formation [cell line]

| PRJNA1028293 | ENA

Smurf1 modulates Smad signaling pathway in fibrotic cataract formation

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

2024-02-14 | GSE245412 | GEO

Genome wide expression change by SMURF1 knocking down in MCF-7 cells

Project description:We aim to the investigate the role of SMURF1 in breast cancer progression. MCF-7 cells were used as the model and SMURF1 was silenced by siRNA.

2018-08-14 | GSE102653 | GEO

Effect of Smurf1 or Smurf2 deficiency on Gene Expression Profiling of aged mouse liver tissues

Project description:Transcriptome analysis of RNAs extracted from livers of wild type or Smurf1 knock out (KO) or Smurf2 KO mice at age of 11 month old. We prepared RNA from the following groups: livers of Wild type (WT) or Smurf1 KO or Smurf2 KO mouse from mixed Black Swiss/129SvEv background at age of 11 month old. The gene expression profiles were compared, and selected genes that showed either increased or decreased expression by a cut-off of 1.5 folds, p< 0.05. The results showed that many genes that are involved in lipid metabolism were upregulated in Smurf1-/- livers. These results also indicate that Smurf1 plays a more prominent role in the liver than Smurf2.

2018-12-19 | GSE113995 | GEO

Characterization of N6-Methyladenosine lncRNAs in sporadic congenital cataract and age-related cataract

Project description:To characterize the N6-methyladenosine (m6A) modification patterns in long non-coding RNAs (lncRNAs) in sporadic congenital cataract (CC) and age-related cataract(ARC).

2024-11-06 | GSE221970 | GEO

Cerebral Cavernous Malformation Proteins and MEKK3 Coordinately Modulate SMURF1 Abundance to Control RhoA-dependent Endothelial Cell Phenotypic State

Project description:Cerebral Cavernous Malformations (CCM), caused by loss of CCM1, CCM2 or CCM3 in endothelial cells (ECs), are leaky capillaries causing seizures and stroke. CCM protein loss gives overlapping changes in biomechanical and transcriptional properties of ECs, due to common RhoA-driven alterations in cytoskeletal organization and intracellular signaling. However, EC models of 3-D tube formation show loss of each CCM protein generates distinct morphological defects in tubular structures. Computational modeling, live-cell imaging and RNA sequencing revealed distinct functional roles of CCM1 and CCM3 in regulating EC-EC and EC-matrix interactions. CCM2 has an intermediate phenotype consistent with its interaction with CCM1 and CCM3. In ECs, CCM proteins regulate SMURF1 E3 ligase ubiquitination and degradation of RhoA. Loss of CCM proteins results in loss of SMURF1 and a concomitant increase of MEKK3, a negative regulator of SMURF1 expression. We propose CCM lesions develop because of dysregulated SMURF1 resulting in RhoA and MEKK3 gain-of-function.

2019-04-05 | GSE112882 | GEO

Expression data from lens epithelial cells (LECs) from Shumiya cataract rats (SCR) with or without cataract (Cat+ or Cat-)

Project description:The Shumiya cataract rat (SCR) is a model for hereditary cataract. Two-third of these rats develop lens opacity within 10-11-weeks. Onset of cataract is attributed to the synergetic effect of lanosterol synthase (Lss) and farnesyl-diphosphate farnesyltransferase 1 (Fdft1) mutant alleles that lead to cholesterol deficiency in the lenses, which in turn adversely affects lens biology including the growth and differentiation of lens epithelial cells (LECs). Nevertheless, the molecular events and changes in gene expression associated with the onset of lens opacity in SCR is poorly understood. Our study aimed to identify the gene expression patterns during cataract formation in SCRs, which may be responsible for cataractogenesis in SCR.

2020-07-31 | GSE152616 | 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