ArticleCirculation research2010
Specific regulation of noncanonical p38alpha activation by Hsp90-Cdc37 chaperone complex in cardiomyocyte.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- P38α deficiency alleviates myocardial ischemia/reperfusion injury by stabilizing c‑Myc to inhibit ferroptosis.Basic research in cardiology · 2026Article
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- HSP90, a Common Therapeutic Target for Suppressing Skin Injury Caused by Exposure to Chemically Diverse Classes of Blistering Agents.The Journal of pharmacology and experimental therapeutics · 2024Article
- PARP1 Promotes Heart Regeneration and Cardiomyocyte Proliferation.International journal of biological sciences · 2024Article
- A Coumarin-Imidazothiadiazole Derivative, SP11 Abrogates Tumor Growth by Targeting HSP90 and Its Client Proteins.Molecules (Basel, Switzerland) · 2023Article
- The Potential of Hsp90 in Targeting Pathological Pathways in Cardiac Diseases.Journal of personalized medicine · 2021Review
- Hsp90 interaction networks in fungi-tools and techniques.FEMS yeast research · 2021Review
- Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021Review
- Hsp90 modulates human sperm capacitation via the Erk1/2 and p38 MAPK signaling pathways.Reproductive biology and endocrinology : RB&E · 2021Article
- Human Hsp90 cochaperones: perspectives on tissue-specific expression and identification of cochaperones with similar in vivo functions.Cell stress & chaperones · 2021Review
- Article
- Therapeutic Effect of Targeting Branched-Chain Amino Acid Catabolic Flux in Pressure-Overload Induced Heart Failure.Journal of the American Heart Association · 2019Article
- Emerging Functions of Human IFIT Proteins in Cancer.Frontiers in molecular biosciences · 2019Review
- The Alpha Isoform of Heat Shock Protein 90 and the Co-chaperones p23 and Cdc37 Promote Opioid Anti-nociception in the Brain.Frontiers in molecular neuroscience · 2019Article
- Sulbactam Protects Hippocampal Neurons Against Oxygen-Glucose Deprivation by Up-Regulating Astrocytic GLT-1 via p38 MAPK Signal Pathway.Frontiers in molecular neuroscience · 2018Article
- Heat-shock protein 90 (Hsp90) promotes opioid-induced anti-nociception by an ERK mitogen-activated protein kinase (MAPK) mechanism in mouse brain.The Journal of biological chemistry · 2017Article
- A systems genetics approach identifiesAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Novel Molecular Strategies and Targets for Opioid Drug Discovery for the Treatment of Chronic Pain.The Yale journal of biology and medicine · 2017Review
- Moderate endoplasmic reticulum stress activates a PERK and p38-dependent apoptosis.Cell stress & chaperones · 2017Article
- p38β Mitogen-Activated Protein Kinase Modulates Its Own Basal Activity by Autophosphorylation of the Activating Residue Thr180 and the Inhibitory Residues Thr241 and Ser261.Molecular and cellular biology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
rationalep38 is an important stress activated protein kinase involved in gene regulation, proliferation, differentiation, and cell death regulation in heart. p38 kinase activity can be induced through canonical pathway via upstream kinases or by noncanonical autophosphorylation. The intracellular p38 kinase activity is tightly regulated and maintained at low level under basal condition. The underlying regulatory mechanism for canonical p38 kinase activation is well-studied, but the regulation of noncanonical p38 autophosphorylation remains poorly understood.
objectiveWe investigated the molecular basis for the regulation of noncanonical p38 autophosphorylation and its potential functional impact in cardiomyocytes. METHODS AND
resultsUsing both proteomic and biochemical tools, we established that heat shock protein (Hsp)90-Cdc37 chaperones are part of the p38alpha signaling complex in mammalian cells both in vitro and in vivo. The Hsp90-Cdc37 chaperone complex interacts with p38 via direct binding between p38 and Cdc37. Cdc37 expression is both sufficient and necessary to suppress noncanonical p38 activation via autophosphorylation at either basal state or under TAB1 (TAK1 binding protein-1) induction. In contrast, Cdc37 expression has no impact on p38 activation by canonical upstream kinase MKK3 or oxidative stress. Furthermore, Hsp90 inhibition results in p38 activation via autophosphorylation, and p38 activity contribute to apoptotic cell death induced by Hsp90 inhibition.
conclusionOur study has revealed a so far uncharacterized function of Hsp90-Cdc37 as an endogenous regulator of noncanonical p38 activity.
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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 OpenQuestion graph.