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Article

MARCKS silencing differentially affects human vascular smooth muscle and endothelial cell phenotypes to inhibit neointimal hyperplasia in saphenous vein.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology - 1 Feb 2009

Monahan Thomas S, Andersen Nicholas D, Martin Michelle C, Malek Junaid Y, Shrikhande Gautam V, Pradhan Leena, Ferran Christiane, LoGerfo Frank W

Abstract excerpt

Intimal hyperplasia (IH) limits the patency of all cardiovascular vein bypass grafts. We previously found the myristoylated alanine-rich C kinase substrate (MARCKS), a key protein kinase C (PKC) substrate, to be up-regulated in canine models of IH. Here, we further characterize the role of MARCKS in IH and examine the phenotypic consequences of MARCKS silencing by small interfering RNA (siRNA) transfection in...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Share to Intracellular Signaling Peptides and Proteins

Share to Muscle, Smooth, Vascular

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Source

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Identifiers

PMID: 18940893
DOI: 10.1096/fj.08-114173
PMCID: PMC2630782

Genes

MARCKS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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