ArticleArteriosclerosis, thrombosis, and vascular biology2013
Kalirin promotes neointimal hyperplasia by activating Rac in smooth muscle cells.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- RamanOmics decodes the spatial vibrational-molecular architecture of senescence in aging and repair.Nature aging · 2026Article
- Identification and characterization of human KALRN mRNA and Kalirin protein isoforms.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Early Injury Landscape in Vein Harvest by Single-Cell and Spatial Transcriptomics.Circulation research · 2024Article
- Integrated single-nuclei and spatial transcriptomic analysis reveals propagation of early acute vein harvest and distension injury signaling pathways following arterial implantation.bioRxiv : the preprint server for biology · 2024Article
- PDGF regulates guanylate cyclase expression and cGMP signaling in vascular smooth muscle.Communications biology · 2022Article
- Association of Thyroid Function with Blood Pressure and Cardiovascular Disease: A Mendelian Randomization.Journal of personalized medicine · 2021Article
- Review
- Kalirin-RAC controls nucleokinetic migration in ADRN-type neuroblastoma.Life science alliance · 2021Article
- Trio family proteins as regulators of cell migration and morphogenesis in development and disease - mechanisms and cellular contexts.Journal of cell science · 2021Review
- Review
- The Emerging Role of Rho Guanine Nucleotide Exchange Factors in Cardiovascular Disorders: Insights Into Atherosclerosis: A Mini Review.Frontiers in cardiovascular medicine · 2021Review
- Regulation of smooth muscle contraction by monomeric non-RhoA GTPases.British journal of pharmacology · 2020Review
- PCARE and WASF3 regulate ciliary F-actin assembly that is required for the initiation of photoreceptor outer segment disk formation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- Genetic Variation of the Kalirin Gene is Associated with ICAS in the Chinese Population.Journal of molecular neuroscience : MN · 2018Article
- Association between Serum Kalirin Levels and theThe journal of Tehran Heart Center · 2018Article
- G908R NOD2 variant in a family with sarcoidosis.Respiratory research · 2018Article
- Sustained Activation of Rho GTPases Promotes a Synthetic Pulmonary Artery Smooth Muscle Cell Phenotype in Neprilysin Null Mice.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Brain Region and Isoform-Specific Phosphorylation Alters Kalirin SH2 Domain Interaction Sites and Calpain Sensitivity.ACS chemical neuroscience · 2017Article
- Using Kalirin conditional knockout mice to distinguish its role in dopamine receptor mediated behaviors.BMC neuroscience · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveKalirin is a multifunctional protein that contains 2 guanine nucleotide exchange factor domains for the GTPases Rac1 and RhoA. Variants of KALRN have been associated with atherosclerosis in humans, but Kalirin's activity has been characterized almost exclusively in the central nervous system. We therefore tested the hypothesis that Kalirin functions as a Rho-guanine nucleotide exchange factor in arterial smooth muscle cells (SMCs). APPROACH AND
resultsKalirin-9 protein is expressed abundantly in aorta and bone marrow, as well as in cultured SMCs, endothelial cells, and macrophages. Moreover, arterial Kalirin was upregulated during early atherogenesis in apolipoprotein E-deficient mice. In cultured SMCs, signaling was affected similarly in 3 models of Kalirin loss-of-function: heterozygous Kalrn deletion, Kalirin RNAi, and treatment with the Kalirin Rho-guanine nucleotide exchange factor -1 inhibitor 1-(3-nitrophenyl)-1H-pyrrole-2,5-dione. With reduced Kalirin function, SMCs showed normal RhoA activation but diminished Rac1 activation, assessed as reduced Rac-GTP levels, p21-activated kinase autophosphorylation, and SMC migration. Kalrn(-/+) SMCs proliferated 30% less rapidly than wild-type SMCs. Neointimal hyperplasia engendered by carotid endothelial denudation was ≈60% less in Kalrn(-/+) and SMC-specific Kalrn(-/+) mice than in control mice.
conclusionsKalirin functions as a guanine nucleotide exchange factor for Rac1 in SMCs, and promotes SMC migration and proliferation both in vitro and in vivo.
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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.