Evidence map›Paper›PMID 24857637›Full record

ArticleVeterinary immunology and immunopathology2014

Myristoylated Alanine Rich C Kinase Substrate (MARCKS) is essential to β2-integrin dependent responses of equine neutrophils.

Mary K Sheats, Kimberly C Pescosolido, Ethan M Hefner, Eui Jae Sung, Kenneth B Adler, Samuel L Jones

Abstract read
In one paragraph

Article in Veterinary immunology and immunopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  5. Article
  6. Targeting Neutrophil βBiomolecules · 2023
    Review
  7. 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 · 2022
    Article
  8. Article
  9. Article
  10. MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Mary K SheatsDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States; Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States. Electronic address: mkpeed@ncsu.edu.
Kimberly C PescosolidoDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States.
Ethan M HefnerDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States.
Eui Jae SungDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States.
Kenneth B AdlerDepartment of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States.
Samuel L JonesDepartment of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States; Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States.
North Carolina State University · US

Funding

Comparative Medicine and Translational Research Training ProgramT32OD011130 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Lauren Virginia Schnabel · 2012 to 2026
$7.8M
Mechanism of Oxidant-Induced Respiratory Mucin SecretionR37HL036982 · NHLBI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI ADLER, KENNETH BRUCE · 2004 to 2013
$4.0M
Interdisciplinary Biomedical Research Training ProgramT35OD011070 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Ronald Hak Long Li · 2012 to 2026
$1.1M
Comparative Medicine and Translational Research Training ProgramT32RR024394 · NCRR · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI JONES, SAMUEL L · 2008 to 2011
$1.1M
TARGETING THE MARCKS-FAMILY PROTEINS TO INHIBIT NEUTROPHIL MIGRATIONK01OD015136 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI SHEATS, MARY KATHERINE · 2012 to 2016
$628k
Interdisciplinary Biomedical Research Training ProgramT35RR025837 · NCRR · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI JONES, SAMUEL L · 2009 to 2011
$103k
NCRR NIH HHS T32 RR024394NCRR NIH HHS T35 RR025837NHLBI NIH HHS R37 HL036982NHLBI NIH HHS R37 HL36982NIH HHS 5K01OD015136NIH HHS K01 OD015136NIH HHS T32 OD011130NIH HHS T35 OD011070
6 · The paper itself

Abstract

Neutrophil infiltration is a prominent feature in a number of pathologic conditions affecting horses including recurrent airway obstruction, ischemia-reperfusion injury, and laminitis. Cell signaling components involved in neutrophil migration represent targets for novel anti-inflammatory therapies. In order to migrate into tissue, neutrophils must respond to chemoattractant signals in their external environment through activation of adhesion receptors (i.e. integrins) and reorganization of the actin cytoskeleton. Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS), a highly conserved actin-binding protein, has a well demonstrated role in cytoskeletal dependent cellular functions (i.e. adhesion, spreading, and migration), but the details of MARCKS involvement in these processes remain vague. We hypothesized that MARCKS serves as a link between the actin cytoskeleton and integrin function in neutrophils. Using a MARCKS-specific inhibitor peptide known as MANS on equine neutrophils in vitro, we demonstrate that inhibition of MARCKS function significantly attenuates β2-integrin-dependent neutrophil functions including migration, adhesion, and immune complex-mediated respiratory burst. The MANS peptide did not, however, inhibit the β2-integrin-independent PMA mediated respiratory burst. These results attest to the essential role of MARCKS function in regulating neutrophil responses, and strongly implicate MARCKS as a potential regulator of β2-integrins in neutrophils.

Indexed as

Amino Acid SequenceAnimalsAntigen-Antibody ComplexCD18 AntigensCell AdhesionCell MovementConserved SequenceHorsesIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesMembrane ProteinsMolecular Sequence DataMyristoylated Alanine-Rich C Kinase SubstrateNeutrophil InfiltrationPeptide FragmentsRespiratory BurstAntigen-Antibody ComplexCD18 AntigensIntracellular Signaling Peptides and ProteinsMARCKS-related peptideMembrane ProteinsMyristoylated Alanine-Rich C Kinase SubstratePeptide FragmentsTetradecanoylphorbol AcetateAdhesionBeta2-integrinInflammationMigrationNeutrophilRespiratory burst

Identifiers

PMID24857637
PMCPMC4108539
OpenAlexW1987011045

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.