ArticleThe Journal of biological chemistry2008
A novel protein kinase A-independent, beta-arrestin-1-dependent signaling pathway for p38 mitogen-activated protein kinase activation by beta2-adrenergic receptors.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 71 citations in OpenAlex.
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- Agonists and hydrogen peroxide mediate hyperoxidation of β2-adrenergic receptor in airway epithelial cells: Implications for tachyphylaxis to β2-agonists in constrictive airway disorders.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Altered CXCR4 dynamics at the cell membrane impairs directed cell migration in WHIM syndrome patients.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Two Non-Visual Arrestins Engage ERK2 Differently.Journal of molecular biology · 2022Article
- Differential Involvement of ACKR3 C-Tail in β-Arrestin Recruitment, Trafficking and Internalization.Cells · 2021Article
- Cysteine redox state regulates human β2-adrenergic receptor binding and function.Scientific reports · 2020Article
- The β2-adrenergic receptor-ROS signaling axis: An overlooked component of β2AR function?Biochemical pharmacology · 2020Review
- G Protein-Coupled Receptor Signaling Through β-Arrestin-Dependent Mechanisms.Journal of cardiovascular pharmacology · 2017Review
- The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2017Review
- Biased G Protein-Coupled Receptor Signaling: New Player in Modulating Physiology and Pathology.Biomolecules & therapeutics · 2017Review
- Multifaceted role of β-arrestins in inflammation and disease.Genes and immunity · 2015Review
- The emerging roles of β-arrestins in fibrotic diseases.Acta pharmacologica Sinica · 2015Review
- Nonhematopoietic β-Arrestin-1 inhibits inflammation in a murine model of polymicrobial sepsis.The American journal of pathology · 2014Article
- Crosstalk between beta-2-adrenoceptor and muscarinic acetylcholine receptors in the airway.Current opinion in pharmacology · 2014Review
- Adrenergic signaling and oxidative stress: a role for sirtuins?Frontiers in physiology · 2013Review
- Apolipoprotein A-I mimetic peptide D-4F promotes human endothelial progenitor cell proliferation, migration, adhesion though eNOS/NO pathway.Molecular biology reports · 2012Article
- Dynamics of the G protein-coupled vasopressin V2 receptor signaling network revealed by quantitative phosphoproteomics.Molecular & cellular proteomics : MCP · 2012Article
- cGMP inhibits TGF-beta signaling by sequestering Smad3 with cytosolic beta2-tubulin in pulmonary artery smooth muscle cells.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Biochemical basis of asthma therapy.The Journal of biological chemistry · 2011Review
- Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling.Trends in biochemical sciences · 2011Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence has demonstrated that p38 mitogen-activated protein kinase (MAPK) has a crucial role in various physiological and pathological processes mediated by beta(2)-adrenergic receptors (beta(2)-ARs). However, the detailed mechanism of beta(2)-ARs-induced p38 MAPK activation has not yet been fully defined. The present study demonstrates a novel kinetic model of p38 MAPK activation induced by beta(2)-ARs in human embryonic kidney 293A cells. The beta(2)-AR agonist isoproterenol induced a time-dependent biphasic phosphorylation of p38 MAPK: the early phase peaked at 10 min, and was followed by a delayed phase that appeared at 90 min and was sustained for 6 h. Interestingly, inhibition of the cAMP/protein kinase A (PKA) pathway failed to affect the early phosphorylation but abolished the delayed activation. By contrast, silencing of beta-arrestin-1 expression by small interfering RNA inhibited the early phase activation of p38 MAPK. Furthermore, the NADPH oxidase complex is a downstream target of beta-arrestin-1, as evidenced by the fact that isoproterenol-induced Rac1 activation was also suppressed by beta-arrestin-1 knockdown. In addition, early phase activation of p38 MAPK was prevented by inactivation of Rac1 and NADPH oxidase by pharmacological inhibitors, overexpression of a dominant negative mutant of Rac1, and p47(phox) knockdown by RNA interference. Of note, we demonstrated that only early activation of p38 MAPK is involved in isoproterenol-induced F-actin rearrangement. Collectively, these data suggest that the classic cAMP/PKA pathway is responsible for the delayed activation, whereas a beta-arrestin-1/Rac1/NADPH oxidase-dependent signaling is a heretofore unrecognized mechanism for beta(2)-AR-mediated early activation of p38 MAPK.
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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.