GLP-1 and diabetic nephropathy share key molecular targets
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Glucagon-like peptide-1 (GLP-1) receptor agonists provide renoprotective benefits in diabetes, yet the molecular mechanisms linking GLP-1 signaling to diabetic nephropathy remain poorly defined. This study aimed to identify shared molecular targets between GLP-1 activity and diabetic kidney disease by integrating protein targets of GLP-1 from UniProt with disease-associated genes from GeneCards. The overlapping gene set was analyzed using STRING and Cytoscape with MCODE clustering, followed by Gene Ontology and KEGG enrichment through the clusterProfiler package. Molecular docking with HADDOCK was employed to validate structural interactions between GLP-1 and central network proteins. We identified 17 shared genes, including STAT3, EP300, MAPK1, and INSR, which formed a densely connected cluster enriched in pathways related to insulin response, hypoxia adaptation, apoptosis, and glucose metabolism. Docking analysis demonstrated direct and favorable binding of GLP-1 to STAT3, PIK3R1, and..., , Title:
# Data from: GLP-1 and diabetic nephropathy share key molecular targets
Authors
Wanderson Gabriel Gomes de Melo¹
Regina Lúcia dos Santos Silva¹
Ianahanna Duarte Santos Soares¹
Bruno de Sousa Barbosa¹
Felipe Cardoso de Brito²
Napoleão Martins Argôlo Neto¹
Dayseanny de Oliveira Bezerra²
Affiliations
¹ Universidade Federal do Piauà (UFPI), Teresina, Brazil
² Instituto Federal do Piauà (IFPI), Teresina, Brazil
Associated Manuscript
Journal: *Canadian Journal of Physiology and Pharmacology*
Manuscript ID: cjpp-2025-0146
Status: Accepted for publication
## Description of Files
csv_and_xlsx/ â Raw and processed data tables (CSV/XLSX) used for network and enrichment analyses.
tsv_and_txt/ â Gene lists, metadata, and formatted text exports from STRING and clusterProfiler outputs.
figures/ â Figures generated for visualization of PPI networks, cluster topology, and enrichment results.
others/ â Supplementary analysis scripts (.R, .py) and notes supporting the dataset.
REA...,
创建时间:
2025-11-04



