Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigating HMGB1 as a Potential Serum Biomarker for Early Diabetic Nephropathy Monitoring by Quantitative Proteomics

ABSTRACT: Current diagnostic methods for diabetic nephropathy (DN) lack precision, especially in early stages and monitoring progression. This study aims to find potential biomarkers for DN progression and evaluate their accuracy. Using serum samples from healthy controls (NC), diabetic patients (DM), early-medium stage DN (DN-EM), and late-stage DN (DN-L), researchers employed quantitative proteomics and Mfuzz clustering analysis revealed 15 proteins showing increased expression during DN progression, hinting at their biomarker potential. Combining Mfuzz clustering with weighted gene co-expression network analysis (WGCNA) highlighted five candidates (HMGB1, CD44, FBLN1, PTPRG, and ADAMTSL4). HMGB1 emerged as a promising biomarker, closely correlated with renal function changes. Experimental validation supported HMGB1’s upregulation under high glucose conditions, reinforcing its potential as an early detection biomarker for DN. This research advances DN understanding and identifies five potential biomarkers, notably HMGB1, as a promising early monitoring target. These findings set the stage for future clinical diagnostic applications in DN.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Serum

SUBMITTER: Lirong Liu

LAB HEAD: Lirong Liu

PROVIDER: PXD047872 | Pride | 2023-12-28

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	RD235ELQ_DM_1.raw	Raw
	RD235ELQ_DM_2.raw	Raw
	RD235ELQ_DM_3.raw	Raw
	RD235ELQ_DM_4.raw	Raw
	RD235ELQ_DM_5.raw	Raw

Items per page:

1 - 5 of 26

Similar Datasets

Identification of mRNAs modulated by knockdown of CD24

Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs. Transcripts upregulated or downregulated by knockdown of CD24 were identified through expression profiling of a total of 12,135 genes in S2-013 CD24 RNAi clones compared to control clones. Before labeling with Cy5 or Cy3, total RNA from two S2-013 CD24 RNAi clones were mixed and total RNA from two control clones were mixed. The supplementary files 'GSE17055_higher_siCD24.txt' and 'GSE17055_higher_control.txt' list the differentially expressed genes.

2010-06-24 | E-GEOD-17055 | biostudies-arrayexpress

Transcription profiling of Xenopus tropicalis wild type and whitehart embryos

Project description:Two batches each of 40 wild type and 40 whitehart sibling embryos were sorted by morphological criteria at stage 37-38, RNA prepped and hybed to arrays. With mutant versus wild type sibling pools. Dyeswaps were performed.

2022-11-21 | E-MEXP-691 | biostudies-arrayexpress

Transcription profiling of zebra fish squint mutant and wild type embryos following a temperature shift in development to investigate environmental and genetic modifiers of squint penetrance

Project description:Environmental and Genetic Modifiers of squint Penetrance during Zebrafish Embryogenesis. Gene expression changes due to temperature shift during devlopment in homozygous squint mutants and wild_type embryos

2006-07-24 | E-MEXP-775 | biostudies-arrayexpress

Identification of differential gene expression modulated by knockdown of MUC1 in MKN45 gastric carcinoma cells

Project description:Transcripts upregulated or downregulated by knockdown of MUC1 were identified through expression profiling of a total of 12,135 genes in comparison with MKN45- MUC1 RNAi clones and control clones. We endeavored to identify genes which expression is affected by MUC1 by performing cDNA microarray analysis on two MKN45 MUC1 RNAi clones and one control clone.

2011-11-15 | E-GEOD-28975 | biostudies-arrayexpress

A small-molecule inhibitor targeting AKR1C1 suppresses cell proliferation and metastasis in non-small cell lung cancer

Project description:Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths, characterized by highly invasion and metastasis. Aldo-keto reductase family 1 member C1 (AKR1C1) plays an important role in cancer cell proliferation and metastasis and has gained attention as an anticancer drug target. Here we report that the natural sesquiterpene lactone alantolactone (ALA) was shown to bind directly to AKR1C1 through the Proteome Integral Solubility Alteration (PISA) analysis, a label-free target identification approach based on thermal proteome profiling.

2022-05-20 | PXD031082 | Pride

Mettl1-mediated B cell responses

Project description:Germinal center (GC) response requires increased protein synthesis. We identify the methyltransferase METTL1 as a translational checkpoint during GC responses. Therefore, we immunized mettl1-cko mice and control mice with NP-OVA, and sorted spleen B cells on day 14.

2024-11-01 | PXD057426 | Pride

Identification of mRNAs modulated by overexpression of N-terminal G3BP

Project description:Transcripts upregulated or downregulated by overexpression of N-terminal G3BP were identified through expression profiling of a total of 12,135 genes in comparison with S2-013 clones in which N-terminal G3BP is overexpressed and control clones. We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism underpinning the observed phenotypic changes by performing cDNA microarray analysis on two S2-013 CD24 RNAi clones and two control clones. Total RNAs from two clones of S2-013 CD24 RNAi or control cells were mixed and used for cDNA microarray analysis.

2010-07-31 | E-GEOD-23342 | biostudies-arrayexpress

Transcriptional profiling of Arabidopsis thaliana grown under arsenate stress

Project description:We examined the changes in gene expression in Arabidopsis thaliana grown under arsenate stress. The transcriptional profiling reveals antioxidant activity and repression of the phosphate starvation response. Keywords: dual label, stress response This experiment included a comparison of three biological replicate controls against three biological arsenate-stressed replicates with a dye-swap technical replicate for a total of six microarray slide hybridizations.

2010-05-26 | E-GEOD-10425 | biostudies-arrayexpress

- Quantitative proteomics pointed out the possible role of the sox system in the interplay between sulphur and arsenic metabolism in the phototroph Halorhodospira halophila

Project description:Study of the photosynthetic metabolism of purple sulphur bacteria Halorhodospira halophila by analysing the proteome of the bacteria cultivated with various sulphur compounds. In this way for the first time a comprehensive sulphur-oxidative photosynthetic network of an Halorhodospiraceaen is presented. As some Ectothiorhodospiraceae have been shown to use arsenite as photosynthetic electron donor, We performed a mass spectrometry-based whole proteome analysis with label-free quantification of H. halophila photoheterotrophically grown in the presence of various inorganic reduced sulphur compounds and in the concomitant presence of sulphide and arsenite, in order to identify proteins (enzymes and electron carriers) involved in its photosynthetic metabolism. Quantitative proteomics revealed that the SoxAXYZB system, typically dedicated to thiosulphate oxidation, is overproduced in this latter growth condition as are two electron carriers, the cytochrome c551/c5 and PioC/HiPIP III. Taken together, these results argue in favour of a chemically-formed thioarsenate oxidized by the Sox system, with c551/c5 and PioC/HiPIP III funnelling electrons towards the Reaction Centre.

2024-04-09 | PXD049262 | Pride

Quantitative proteomics and RNA-sequencing of mouse liver endothelial cells identify novel regulators of BMP6 by iron

Project description:Iron induces hepcidin by activating bone morphogenetic protein (BMP)6-SMAD signaling. Liver endothelial cells (LECs) produce BMP6, but the molecular mechanisms are incompletely understood. To address this, we performed proteomics and RNA-sequencing on LECs from iron-adequate and iron-loaded mice. Gene set enrichment analysis identified transcription factors activated by high iron, including Nrf-2, which was previously reported to contribute to BMP6 regulation, and proto-oncogene c-Jun (encoded by Jun). Jun knockdown blocked Bmp6, but not Nrf-2 pathway, induction by iron in LEC cultures. Moreover, chromatin immunoprecipitation of mouse livers showed iron-dependent c-Jun binding to predicted sites in Bmp6 regulatory regions. Finally, c-Jun inhibitor blunted induction of Bmp6 and hepcidin, but not Nrf-2 activity, in iron-loaded mice. However, Bmp6 expression and iron parameters were unchanged in endothelial Jun knockout mice. Our data suggest that c-Jun participates in iron-mediated BMP6 regulation independent of Nrf-2, though the mechanisms may be redundant and/or multifactorial.

2023-12-28 | PXD039830 | 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