ArticleArteriosclerosis, thrombosis, and vascular biology2008
Gas6-axl receptor signaling is regulated by glucose in vascular smooth muscle cells.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 57 citations in OpenAlex.
- Preclinical evaluation of CPL423: a novel potent small-molecule inhibitor of TAM family and FLT3 kinase for cancer therapy.Frontiers in pharmacology · 2026Article
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- PFKP silencing suppresses tumor growth via the AXL-MET axis.International journal of biological sciences · 2024Article
- AXL receptor tyrosine kinase modulates gonadotropin-releasing hormone receptor signaling.Cell communication and signaling : CCS · 2023Article
- AXL/Gas6 signaling mechanisms in the hypothalamic-pituitary-gonadal axis.Frontiers in endocrinology · 2023Review
- Sex-Stratified Gene Regulatory Networks Reveal Female Key Driver Genes of Atherosclerosis Involved in Smooth Muscle Cell Phenotype Switching.Circulation · 2021Article
- TAM receptors in cardiovascular disease.Cardiovascular research · 2019Review
- AXL phosphorylates and up-regulates TNS2 and its implications in IRS-1-associated metabolism in cancer cells.Journal of biomedical science · 2018Article
- HGF-induced formation of the MET-AXL-ELMO2-DOCK180 complex promotes RAC1 activation, receptor clustering, and cancer cell migration and invasion.The Journal of biological chemistry · 2018Article
- Role of Receptor Tyrosine Kinase Signaling in Renal Fibrosis.International journal of molecular sciences · 2016Review
- Autophagy in cardiovascular biology.The Journal of clinical investigation · 2015Review
- Axl as a mediator of cellular growth and survival.Oncotarget · 2014Review
- High glucose induces human endothelial dysfunction through an Axl-dependent mechanism.Cardiovascular diabetology · 2014Article
- Biology of the TAM receptors.Cold Spring Harbor perspectives in biology · 2013Review
- Article
- Axl-dependent signalling: a clinical update.Clinical science (London, England : 1979) · 2012Review
- Novel tyrosine kinase signaling pathways: implications in vascular remodeling.Current opinion in nephrology and hypertension · 2012Review
- Glycoxidised LDL induced the upregulation of Axl receptor tyrosine kinase and its ligand in mouse mesangial cells.PloS one · 2012Article
- Plasma protein growth arrest-specific 6 levels are associated with altered glucose tolerance, inflammation, and endothelial dysfunction.Diabetes care · 2010Article
- Gas6-Axl pathway: the role of redox-dependent association of Axl with nonmuscle myosin IIB.Hypertension (Dallas, Tex. : 1979) · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe receptor tyrosine kinase Axl and its ligand Gas6 are involved in the development of renal diabetic disease. In vascular smooth muscle cells (VSMCs) Axl is activated by reactive oxygen species and stimulates migration and cell survival, suggesting a role for Axl in the vascular complications of diabetes. METHODS AND
resultsWe investigated the effect of varying glucose concentration on Axl signaling in VSMCs. Glucose exerted powerful effects on Gas6-Axl signaling with greater activation of Akt and mTOR in low glucose, and greater activation of ERK1/2 in high glucose. Plasma membrane distribution and tyrosine phosphorylation of Axl were not affected by glucose. However, coimmunoprecipitation studies demonstrated that glucose changed the interaction of Axl with its binding partners. Specifically, binding of Axl to the p85 subunit of PI3-kinase was increased in low glucose, whereas binding to SHP-2 was increased in high glucose. Furthermore, Gas6-Axl induced migration was increased in high glucose, whereas Gas6-Axl mediated inhibition of apoptosis was greater in low glucose.
conclusionsThis study demonstrates a role for glucose in altering Axl signaling through coupling to binding partners and suggests a mechanism by which Axl contributes to VSMC dysfunction in diabetes.
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Registered trials
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.