ArticleLife science alliance2024
Interrogating endothelial barrier regulation by temporally resolved kinase network generation.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Host kinase regulation of Plasmodium vivax dormant and replicating liver stages.PLoS neglected tropical diseases · 2026Article
- Active Endothelial Inactivation of Hyperpermeability: The Role of Nitric Oxide-Driven cAMP/Epac1 Signaling.Journal of cardiovascular development and disease · 2025Review
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- Using machine learning to dissect host kinases required for Leishmania internalization and development.Molecular and biochemical parasitology · 2024Article
- Systems-level reconstruction of kinase phosphosignaling networks regulating endothelial barrier integrity using temporal data.NPJ systems biology and applications · 2024Article
- Systems-level reconstruction of kinase phosphosignaling networks regulating endothelial barrier integrity using temporal data.bioRxiv : the preprint server for biology · 2024Article
- Using machine learning to dissect host kinases required forbioRxiv : the preprint server for biology · 2024Article
- Multiple receptor tyrosine kinases regulate dengue infection of hepatocytes.Frontiers in cellular and infection microbiology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Kinases are key players in endothelial barrier regulation, yet their temporal function and regulatory phosphosignaling networks are incompletely understood. We developed a novel methodology, Temporally REsolved KInase Network Generation (TREKING), which combines a 28-kinase inhibitor screen with machine learning and network reconstruction to build time-resolved, functional phosphosignaling networks. We demonstrated the utility of TREKING for identifying pathways mediating barrier integrity after activation by thrombin with or without TNF preconditioning in brain endothelial cells. TREKING predicted over 100 kinases involved in barrier regulation and discerned complex condition-specific pathways. For instance, the MAPK-activated protein kinase 2 (MAPKAPK2/MK2) had early barrier-weakening activity in both inflammatory conditions but late barrier-strengthening activity exclusively with thrombin alone. Using temporal Western blotting, we confirmed that MAPKAPK2/MK2 was differentially phosphorylated under the two inflammatory conditions. We further showed with lentivirus-mediated knockdown of MAPK14/p38α and drug targeting the MAPK14/p38α-MAPKAPK2/MK2 complex that a MAP3K20/ZAK-MAPK14/p38α axis controlled the late activation of MAPKAPK2/MK2 in the thrombin-alone condition. Beyond the MAPKAPK2/MK2 switch, TREKING predicts extensive interconnected networks that control endothelial barrier dynamics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.