The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration.

Background: Metabolic syndrome represents a pancreatic ductal adenocarcinoma (PDAC) risk factor. Metabolic alterations favor PDAC onset, which occurs early upon dysmetabolism. Pancreatic neoplastic lesions evolve within a dense desmoplastic stroma, consisting in abundant extracellular matrix settled by cancer associated fibroblasts (CAFs).

Complex portal 2025: predicted human complexes and enhanced visualisation tools for the comparison of orthologous and paralogous complexes.

The Complex Portal (www.ebi.ac.

IntAct Database for Accessing IMEx's Contextual Metadata of Molecular Interactions.

The International Molecular Exchange Consortium (IMEx) has evolved into a vital partnership of open resources dedicated to curating molecular interaction data from the scientific literature. This consortium, which includes IntAct, MINT, MatrixDB, and DIP, is a collaborative effort with a central mission of aggregating detailed molecular interaction experimental evidence in a machine-readable format, supported by controlled vocabularies and standard ontologies. The IntAct molecular interaction database (www.

SignalingProfiler 2.0 a network-based approach to bridge multi-omics data to phenotypic hallmarks.

Unraveling how cellular signaling is remodeled upon perturbation is crucial for understanding disease mechanisms and identifying potential drug targets. In this pursuit, computational tools generating mechanistic hypotheses from multi-omics data have invaluable potential. Here, we present a newly implemented version (2.

Stage-dependent phosphoproteome remodeling of Parkinson's disease blood cells.

The complexity and heterogeneity of PD necessitate advanced diagnostic and prognostic tools to elucidate its molecular mechanisms accurately. In this study, we addressed this challenge by conducting a pilot phospho-proteomic analysis of peripheral blood mononuclear cells (PBMCs) from idiopathic PD patients at varying disease stages to delineate the functional alterations occurring in these cells throughout the disease course and identify key molecules and pathways contributing to PD progression. By integrating clinical data with phospho-proteomic profiles across various PD stages, we identify potential stage-specific molecular signatures indicative of disease progression.