ArticleNature communications2015
Disruption of p21-activated kinase 1 gene diminishes atherosclerosis in apolipoprotein E-deficient mice.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 45 citations in OpenAlex.
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- Glucose-Regulated Protein 78, via Releasing β-Catenin from Adherens Junctions, Facilitates Its Interaction with STAT3 in Mediating Retinal Neovascularization.The American journal of pathology · 2024Article
- Requirement of Site-Specific Tyrosine Phosphorylation of Cortactin in Retinal Neovascularization and Vascular Leakage.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
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- Novel Role of Prereplication Complex Component Cell Division Cycle 6 in Retinal Neovascularization.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- P21 activated kinase-1 (PAK1) in macrophages is required for promotion of Th17 cell response during helminth infection.Journal of cellular and molecular medicine · 2020Article
- PKCθ-JunB axis via upregulation of VEGFR3 expression mediates hypoxia-induced pathological retinal neovascularization.Cell death & disease · 2020Article
- Identification of Biological Pathways Contributing to Marbling in Skeletal Muscle to Improve Beef Cattle Breeding.Frontiers in genetics · 2019Article
- p115 RhoGEF activates the Rac1 GTPase signaling cascade in MCP1 chemokine-induced vascular smooth muscle cell migration and proliferation.The Journal of biological chemistry · 2017Article
- Visualization of endothelial barrier damage prior to formation of atherosclerotic plaques.Histochemistry and cell biology · 2017Article
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- PLCβ3 mediates cortactin interaction with WAVE2 in MCP1-induced actin polymerization and cell migration.Molecular biology of the cell · 2015Article
- Cyclic AMP Response Element Binding Protein Mediates Pathological Retinal Neovascularization via Modulating DLL4-NOTCH1 Signaling.EBioMedicine · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pak1 plays an important role in various cellular processes, including cell motility, polarity, survival and proliferation. To date, its role in atherogenesis has not been explored. Here we report the effect of Pak1 on atherogenesis using atherosclerosis-prone apolipoprotein E-deficient (ApoE(-/-)) mice as a model. Disruption of Pak1 in ApoE(-/-) mice results in reduced plaque burden, significantly attenuates circulating IL-6 and MCP-1 levels, limits the expression of adhesion molecules and diminishes the macrophage content in the aortic root of ApoE(-/-) mice. We also observed reduced oxidized LDL uptake and increased cholesterol efflux by macrophages and smooth muscle cells of ApoE(-/-):Pak1(-/-) mice as compared with ApoE(-/-) mice. In addition, we detect increased Pak1 phosphorylation in human atherosclerotic arteries, suggesting its role in human atherogenesis. Altogether, these results identify Pak1 as an important factor in the initiation and progression of atherogenesis.
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