ArticleThe Journal of biological chemistry2012
Angiotensin-II and MARCKS: a hydrogen peroxide- and RAC1-dependent signaling pathway in vascular endothelium.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Role for the PIPJournal of cell communication and signaling · 2024Review
- Targeting N-Myristoylation Through NMT2 Prevents Cardiac Hypertrophy and Heart Failure.JACC. Basic to translational science · 2023Article
- MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Dissecting in vivo and in vitro redox responses using chemogenetics.Free radical biology & medicine · 2021Review
- Restoration of MARCKS enhances chemosensitivity in cancer.Journal of cancer research and clinical oncology · 2020Article
- Small GTPases and Their Role in Vascular Disease.International journal of molecular sciences · 2019Review
- Literature-Based Enrichment Insights into Redox Control of Vascular Biology.Oxidative medicine and cellular longevity · 2019Review
- MARCKS and MARCKS-like proteins in development and regeneration.Journal of biomedical science · 2018Review
- MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells.The Journal of veterinary medical science · 2016Article
- Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.Molecular biology of the cell · 2016Article
- Reverse Signaling by Semaphorin-6A Regulates Cellular Aggregation and Neuronal Morphology.PloS one · 2016Article
- Myristoylated Alanine-Rich Protein Kinase Substrate (MARCKS) Regulates Small GTPase Rac1 and Cdc42 Activity and Is a Critical Mediator of Vascular Smooth Muscle Cell Migration in Intimal Hyperplasia Formation.Journal of the American Heart Association · 2015Article
- Tumor cell migration screen identifies SRPK1 as breast cancer metastasis determinant.The Journal of clinical investigation · 2015Article
- Inhibition of cellular methyltransferases promotes endothelial cell activation by suppressing glutathione peroxidase 1 protein expression.The Journal of biological chemistry · 2014Article
- Central role for hydrogen peroxide in P2Y1 ADP receptor-mediated cellular responses in vascular endothelium.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Reactive oxygen species, vascular Noxs, and hypertension: focus on translational and clinical research.Antioxidants & redox signaling · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
MARCKS is an actin-binding protein that modulates vascular endothelial cell migration and cytoskeleton signaling (Kalwa, H., and Michel, T. (2011) J. Biol. Chem. 286, 2320-2330). Angiotensin-II is a vasoactive peptide implicated in vascular physiology as well as pathophysiology; the pathways connecting angiotensin-II and cytoskeletal remodeling are incompletely understood. Here we show that MARCKS is expressed in intact arterial preparations, with prominent staining of the endothelium. In endothelial cells, angiotensin-II-promoted MARCKS phosphorylation is abrogated by PEG-catalase, implicating endogenous H(2)O(2) in the angiotensin-II response. Studies using the H(2)O(2) biosensor HyPer2 reveal that angiotensin-II promotes increases in intracellular H(2)O(2). We used a Rac1 FRET biosensor to show that angiotensin-II promotes Rac1 activation that is attenuated by PEG-catalase. siRNA-mediated Rac1 knockdown blocks angiotensin-II-stimulated MARCKS phosphorylation. Cell imaging studies using a phosphoinositide 4,5-bisphosphate (PIP(2)) biosensor revealed that angiotensin-II PIP(2) regulation depends on MARCKS and H(2)O(2). siRNA-mediated knockdown of MARCKS or Rac1 attenuates receptor-mediated activation of the tyrosine kinase c-Abl and disrupts actin fiber formation. These studies establish a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.
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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.