ArticleMolecular therapy : the journal of the American Society of Gene Therapy2013
Disruption of TAB1/p38α interaction using a cell-permeable peptide limits myocardial ischemia/reperfusion injury.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling.Acta pharmacologica Sinica · 2023Article
- Characterization of p38α autophosphorylation inhibitors that target the non-canonical activation pathway.Nature communications · 2023Article
- Fluorescence resonance energy transfer (FRET) spatiotemporal mapping of atypical P38 reveals an endosomal and cytosolic spatial bias.Scientific reports · 2023Article
- Diversity and versatility of p38 kinase signalling in health and disease.Nature reviews. Molecular cell biology · 2021Review
- Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021Review
- Communication Between Cardiomyocytes and Fibroblasts During Cardiac Ischemia/Reperfusion and Remodeling: Roles of TGF-β, CTGF, the Renin Angiotensin Axis, and Non-coding RNA Molecules.Frontiers in physiology · 2021Review
- G protein-coupled receptors activate p38 MAPK via a non-canonical TAB1-TAB2- and TAB1-TAB3-dependent pathway in endothelial cells.The Journal of biological chemistry · 2019Article
- Ubiquitination as a Key Regulator of Endosomal Signaling by GPCRs.Frontiers in cell and developmental biology · 2019Review
- Ubiquitin plays an atypical role in GPCR-induced p38 MAP kinase activation on endosomes.The Journal of cell biology · 2015Article
- RACK1 antagonizes TNF-α-induced cell death by promoting p38 activation.Scientific reports · 2015Article
- p38 MAPK in cardioprotection - are we there yet?British journal of pharmacology · 2015Review
- Good and bad sides of TGFβ-signaling in myocardial infarction.Frontiers in physiology · 2015Review
- Joint clustering of protein interaction networks through Markov random walk.BMC systems biology · 2014Article
Corrections and comments
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Authors and funding
15 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting the adaptor protein (transforming growth factor-β (TGF-β)-activated protein kinase 1 (TAK1)-binding protein 1) (TAB1)-mediated non-canonical activation of p38α to limit ischemia/reperfusion (I/R) injury after an acute myocardial infarction seems to be attractive since TAB1/p38α interaction occurs specifically in very limited circumstances and possesses unique structural basis. However, so far no TAB1/p38α interaction inhibitor has been reported due to the limited knowledge about the interfaces. In this study, we sought to identify key amino acids essential for the unique mode of interaction with computer-guided molecular simulations and molecular docking. After validation of the predicted three-dimensional (3-D) structure of TAB1/p38α complex, we designed several peptides and evaluated whether they could block TAB1/p38α interaction with selectivity. We found that a cell-permeable peptide worked as a selective TAB1/p38α interaction inhibitor and decreased myocardial I/R injury. To our knowledge, this is the first TAB1/p38α interaction inhibitor.
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Registered trials
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