ArticleInflammation2015
In Vitro Neutrophil Migration Requires Protein Kinase C-Delta (δ-PKC)-Mediated Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Phosphorylation.
Article in Inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Co-expression of MARCKS and GSDMD pathway genes in tuberculous meningitis: a multi-omics analysis of blood-brain barrier disruption.Frontiers in cellular and infection microbiology · 2026Article
- Article
- NAC couples protein synthesis with nascent polypeptide myristoylation on the ribosome.The EMBO journal · 2025Article
- MARCKS protein is a potential target in a naturally occurring equine model of neutrophilic asthma.Respiratory research · 2025Article
- MARCKS Inhibition Alters Bovine Neutrophil Responses toBiomedicines · 2024Article
- A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in βCell adhesion & migration · 2023Article
- PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023Review
- Myristoylated, alanine-rich C-kinase substrate (MARCKS) regulates toll-like receptor 4 signaling in macrophages.Scientific reports · 2023Article
- Phenotypic Variability in PRKCD: a Review of the Literature.Journal of clinical immunology · 2023Review
- TFEB: a double-edged sword for tumor metastasis.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Review
- Review
- MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type.Antioxidants (Basel, Switzerland) · 2022Article
- Peptide Inhibitors of MARCKS Suppress Endotoxin Induced Uveitis in Rats.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2022Article
- The myristoylated alanine-rich C-kinase substrates (MARCKS): A membrane-anchored mediator of the cell function.Autoimmunity reviews · 2021Review
- Pathophysiological roles of myristoylated alanine-rich C-kinase substrate (MARCKS) in hematological malignancies.Biomarker research · 2021Review
- Pro-Resolving FPR2 Agonists Regulate NADPH Oxidase-Dependent Phosphorylation of HSP27, OSR1, and MARCKS and Activation of the Respective Upstream Kinases.Antioxidants (Basel, Switzerland) · 2021Article
- MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells.Oncology letters · 2020Article
- MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019Review
- MARCKS and MARCKS-like proteins in development and regeneration.Journal of biomedical science · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Dysregulated release of neutrophil reactive oxygen species and proteolytic enzymes contributes to both acute and chronic inflammatory diseases. Therefore, molecular regulators of these processes are potential targets for new anti-inflammatory therapies. We have shown previously that myristoylated alanine-rich C-kinase substrate (MARCKS), a well-known actin binding protein and protein kinase C (PKC) substrate, is a key regulator of neutrophil functions. In the current study, we investigate the role of PKC-mediated MARCKS phosphorylation in neutrophil migration and adhesion in vitro. We report that treatment of human neutrophils with the δ-PKC inhibitor rottlerin significantly attenuates f-Met-Leu-Phe (fMLF)-induced MARCKS phosphorylation (IC50=5.709 μM), adhesion (IC50=8.4 μM), and migration (IC50=6.7 μM), while α-, β-, and ζ-PKC inhibitors had no significant effect. We conclude that δ-PKC-mediated MARCKS phosphorylation is essential for human neutrophil migration and adhesion in vitro. These results implicate δ-PKC-mediated MARCKS phosphorylation as a key step in the inflammatory response of neutrophils.
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What OpenQuestion holds
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.