ArticleNature communications2023
Characterization of p38α autophosphorylation inhibitors that target the non-canonical activation pathway.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Mapping of dynamic allostery within p38 alpha kinase via network analyses and NMR spectroscopy.Nature communications · 2026Article
- Neural Excitation-Inhibition Imbalance in Cervical Spondylotic Myelopathy.Communications medicine · 2026Article
- Exercise and CD8Journal of molecular medicine (Berlin, Germany) · 2026Review
- Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Role of Atypical MAPK p38 Signaling in the Progression of Influenza A-Induced Acute Lung Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Neuropilin Antagonists (NRPas) Block the Phosphorylation of the Cancer Therapeutic Key Factor p38α Kinase Triggering Cell Death.Molecules (Basel, Switzerland) · 2025Article
- Quantification of Binding of Small Molecules to Native Proteins Overexpressed in Living Cells.Journal of the American Chemical Society · 2024Article
- Calciprotein Particles Induce Cellular Compartment-Specific Proteome Alterations in Human Arterial Endothelial Cells.Journal of cardiovascular development and disease · 2023Article
- Structural basis of a redox-dependent conformational switch that regulates the stress kinase p38α.Nature communications · 2023Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p38α is a versatile protein kinase that can control numerous processes and plays important roles in the cellular responses to stress. Dysregulation of p38α signaling has been linked to several diseases including inflammation, immune disorders and cancer, suggesting that targeting p38α could be therapeutically beneficial. Over the last two decades, numerous p38α inhibitors have been developed, which showed promising effects in pre-clinical studies but results from clinical trials have been disappointing, fueling the interest in the generation of alternative mechanisms of p38α modulation. Here, we report the in silico identification of compounds that we refer to as non-canonical p38α inhibitors (NC-p38i). By combining biochemical and structural analyses, we show that NC-p38i efficiently inhibit p38α autophosphorylation but weakly affect the activity of the canonical pathway. Our results demonstrate how the structural plasticity of p38α can be leveraged to develop therapeutic opportunities targeting a subset of the functions regulated by this pathway.
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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 Socratic graph.