ArticlePloS one2018
A type 2 diabetes disease module with a high collective influence for Cdk2 and PTPLAD1 is localized in endosomes.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- HACD3 promotes malignant progression of NSCLC by suppressing the MKK7/MAPK10 signaling axis.BMC cancer · 2025Article
- Acidic Nanoparticles Restore Lysosomal Acidification and Rescue Metabolic Dysfunction in Pancreatic β-Cells under Lipotoxic Conditions.ACS nano · 2024Article
- PTPLAD1 Regulates PHB-Raf Interaction to Orchestrate Epithelial-Mesenchymal and Mitofusion-Fission Transitions in Colorectal Cancer.International journal of biological sciences · 2024Article
- Genome-Wide Association Studies Reveal Candidate Genes Associated with Pigmentation Patterns of Single Feathers of Tianfu Nonghua Ducks.Animals : an open access journal from MDPI · 2023Article
- Identification of autophagy-related genes as potential biomarkers for type 1 diabetes mellitus.Annals of translational medicine · 2022Article
- Insulin's Discovery: New Insights on Its Hundredth Birthday: From Insulin Action and Clearance to Sweet Networks.International journal of molecular sciences · 2021Review
- Network medicine-travelling with the insulin receptor: Encounter of the second type.EClinicalMedicine · 2019Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the identification of many susceptibility genes our knowledge of the underlying mechanisms responsible for complex disease remains limited. Here, we identified a type 2 diabetes disease module in endosomes, and validate it for functional relevance on selected nodes. Using hepatic Golgi/endosomes fractions, we established a proteome of insulin receptor-containing endosomes that allowed the study of physical protein interaction networks on a type 2 diabetes background. The resulting collated network is formed by 313 nodes and 1147 edges with a topology organized around a few major hubs with Cdk2 displaying the highest collective influence. Overall, 88% of the nodes are associated with the type 2 diabetes genetic risk, including 101 new candidates. The Type 2 diabetes module is enriched with cytoskeleton and luminal acidification-dependent processes that are shared with secretion-related mechanisms. We identified new signaling pathways driven by Cdk2 and PTPLAD1 whose expression affects the association of the insulin receptor with TUBA, TUBB, the actin component ACTB and the endosomal sorting markers Rab5c and Rab11a. Therefore, the interactome of internalized insulin receptors reveals the presence of a type 2 diabetes disease module enriched in new layers of feedback loops required for insulin signaling, clearance and islet biology.
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