ArticleBritish journal of pharmacology2010
Angiogenesis: a new physiological role for N-arachidonoyl serine and GPR55?
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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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
3 citing papers in PubMed, 13 citations in OpenAlex.
- The role of the metabolite cargo of extracellular vesicles in tumor progression.Cancer metastasis reviews · 2021Review
- Enabling Metabolomics Based Biomarker Discovery Studies Using Molecular Phenotyping of Exosome-Like Vesicles.PloS one · 2016Article
- CB2 receptor activation inhibits melanoma cell transmigration through the blood-brain barrier.International journal of molecular sciences · 2014Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
N-arachidonoyl serine (ARA-S) is one of a number of acyl amino acids recently identified in mammalian tissues. It has been referred to as an endocannabinoid-like lipid largely based on its structural similarities with the endocannabinoid, N-arachidonoyl ethanolamide (anandamide). However, little is known about its potential physiological functions and receptor targets. In this issue of the British Journal of Pharmacology, Zhang and colleagues show that ARA-S is a potent inducer of endothelial cell proliferation and migration, and angiogenesis in vitro. Furthermore, this pro-angiogenic action is mediated, at least partly, by activation of the poorly characterized, G-protein-coupled GPR55 receptor. ARA-S, via GPR55, increases phosphorylation of extracellular signal-regulated kinases and Akt, and vascular endothelial growth factor signalling. These exciting findings highlight the endothelium as an endogenous target for ARA-S and GPR55.
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