Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Novel targets in renal fibrosis based on bioinformatic analysis II

ABSTRACT: Novel targets in renal fibrosis based on bioinformatic analysis II

PROVIDER: PRJNA899899 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22247629.fastq.gz	Fastqsanger.gz
	SRR22247630.fastq.gz	Fastqsanger.gz
	SRR22247631.fastq.gz	Fastqsanger.gz
	SRR22247632.fastq.gz	Fastqsanger.gz
	SRR22247633.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Novel targets in renal fibrosis based on bioinformatic analysis I

Project description:Novel targets in renal fibrosis based on bioinformatic analysis I

| PRJNA899890 | ENA

Novel targets in renal fibrosis based on bioinformatic analysis II

Project description:Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under UUO model in mouse kidneys were investigated by integrating two transcriptional data profiles.

2023-01-06 | GSE217654 | GEO

Novel targets in renal fibrosis based on bioinformatic analysis I

2023-01-06 | GSE217650 | GEO

Novel targets in renal fibrosis based on bioinformatic analysis.

Project description:Background: Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under unilateral ureteral obstruction (UUO) model in mouse kidneys were investigated by integrating two transcriptional data profiles. Methods: The mice were exposed to UUO surgery in two independent experiments. After 7 days, two datasets were sequenced from mice kidney tissues, respectively, and the transcriptome data were analyzed to identify the differentially expressed genes (DEGs). Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were executed. A Protein-Protein Interaction (PPI) network was constructed based on an online database STRING. Additionally, hub genes were identified and shown, and their expression levels were investigated in a public dataset and confirmed by quantitative real time-PCR (qRT-PCR) in vivo. Results: A total of 537 DEGs were shared by the two datasets. GO and the KEGG analysis showed that DEGs were typically enriched in seven pathways. Specifically, five hub genes (Bmp1, CD74, Fcer1g, Icam1, H2-Eb1) were identified by performing the 12 scoring methods in cytoHubba, and the receiver operating characteristic (ROC) curve indicated that the hub genes could be served as biomarkers. Conclusion: A gene network reflecting the transcriptome signature in CKD was established. The five hub genes identified in this study are potentially useful for the treatment and/or diagnosis CKD as biomarkers.

| S-EPMC9745177 | biostudies-literature

HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury

Project description:HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury

| PRJNA1148650 | ENA

HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury

Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we transfected TKPTS cells with Hnf3a overexpression plasmids or control plasmids, and then performed transcriptome sequencing.

2025-03-01 | GSE274962 | GEO

HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α (also known as FOXA1) expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we analyse the genome-wide target sites of HNF3α using CUT&Tag sequencing.

2025-03-01 | GSE274963 | GEO

miR-132 mediates renal fibrosis

Project description:miR-132 mediates renal fibrosis

| PRJNA307696 | ENA

HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

Project description:HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

| PRJNA1148649 | ENA

Proteomic analysis of renal biomarkers of kidney allograft fibrosis – a study in renal transplant patients

Project description:Renal transplantation is the preferred treatment of end stage renal disease, but allograft survival is limited by development of interstitial fibrosis and tubular atrophy in response to various stimuli. Much effort has been put into identifying new protein markers of fibrosis to support the diagnosis. In present work, we performed an in-depth quantitative proteomics analysis of allograft biopsies from 31 prevalent renal transplant patients and identified correlated the quantified proteins with the volume fraction of fibrosis as determined by a morphometric method. Linear regression analysis identified four proteins that were highly associated with the degree of interstitial fibrosis, namely Coagulation Factor XIII A chain (estimate 18.7, adjusted p<0.03), Uridine Phosphorylase 1 (estimate 19.4, adjusted p<0.001), Actin-related protein 2/3 subunit 2 (estimate 34.2, adjusted p<0.05) and Cytochrome C Oxidase Assembly Factor 6 homolog (estimate -44.9, adjusted p<0.002) even after multiple testing. Proteins that were negatively associated with fibrosis (p < 0.005) were primarily related to normal metabolic processes and respiration, whereas proteins that were positively associated with fibrosis (p < 0.005) were involved in catabolic processes, cytoskeleton organization and immune response. The identified proteins may be candidates for further validation with regards to renal fibrosis. The results support the notion that cytoskeleton organization and immune responses are prevalent processes in renal allograft fibrosis.

2020-05-26 | PXD017867 | Pride

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