ArticleAmerican journal of respiratory cell and molecular biology2010
Myristoylated alanine-rich C-kinase substrate (MARCKS) protein regulation of human neutrophil migration.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 66 citations in OpenAlex.
- Plasma proteomic profiling of septic shock and acute pancreatitis identifies shared signatures and disease-specific pathways.Scientific reports · 2026Article
- Structural diversity of lipid A modulates neutrophil proteome and secretome responses.Journal of proteomics · 2026Article
- Aging changes the mechanism that underlies JAK2 modulation of neutrophil function.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Bioinformatics characterization and tissue-specific expression of MARCKS and MLP genes in the regenerating salamander Cynops orientalis.Molecular genetics and genomics : MGG · 2026Article
- MARCKS N-terminal sequence-derived inhibitor peptides impair monocytic ROS production and migration via MARCKS-independent effects.Molecular biology reports · 2025Article
- MARCKS protein is a potential target in a naturally occurring equine model of neutrophilic asthma.Respiratory research · 2025Article
- Neutrophil elastase promotes mucin secretion in airway epithelial cells through the MARCKS/ACK1/cortactin pathway.Central-European journal of immunology · 2025Article
- A peptide against the N-terminus of myristoylated alanine-rich C kinase substrate promotes neuronal differentiation in SH-SY5Y human neuroblastoma cells.The Journal of veterinary medical science · 2024Article
- MARCKS Inhibition Alters Bovine Neutrophil Responses toBiomedicines · 2024Article
- Distinct functional neutrophil phenotypes in sepsis patients correlate with disease severity.Frontiers in immunology · 2024Article
- A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in βCell adhesion & migration · 2023Article
- Myristoylated, alanine-rich C-kinase substrate (MARCKS) regulates toll-like receptor 4 signaling in macrophages.Scientific reports · 2023Article
- Targeting Neutrophil βBiomolecules · 2023Review
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- MARCKS Is an Essential Regulator of Reactive Oxygen Species Production in the Monocytic Cell Type.Antioxidants (Basel, Switzerland) · 2022Article
- Phosphorylation-dependent proteome of Marcks in ependyma during aging and behavioral homeostasis in the mouse forebrain.GeroScience · 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
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neutrophil migration into infected tissues is essential for host defense, but products of activated neutrophils can be quite damaging to host cells. Neutrophil influx into the lung and airways and resultant inflammation characterizes diseases such as chronic obstructive pulmonary disease, bronchiectasis, and cystic fibrosis. To migrate, neutrophils must reorganize the actin cytoskeleton to establish a leading edge pseudopod and a trailing edge uropod. The actin-binding protein myristoylated alanine-rich C-kinase substrate (MARCKS) has been shown to bind and cross-link actin in a variety of cell types and to co-localize with F-actin in the leading edge lamellipodium of migrating fibroblasts. The hypothesis that MARCKS has a role in the regulation of neutrophil migration was tested using a cell-permeant peptide derived from the MARCKS myristoylated aminoterminus (MANS peptide). Treatment of isolated human neutrophils with MANS significantly inhibited both their migration and beta2 integrin-dependent adhesion in response to N-formyl-methionyl-leucyl-phenylalanine (fMLF), IL-8, or leukotriene (LT)B(4). The IC(50) for fMLF-induced migration and adhesion was 17.1 microM and 12.5 microM, respectively. MANS significantly reduced the F-actin content in neutrophils 30 seconds after fMLF stimulation, although the peptide did not alter the ability of cells to polarize or spread. MANS did not alter fMLF-induced increases in surface beta2 integrin expression. These results suggest that MARCKS, via its myristoylated aminoterminus, is a key regulator of neutrophil migration and adhesion.
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Registered trials
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