[1] SUSAN M. HUANG. Identification of a New Class of Molecules, the Arachidonyl Amino Acids, and Characterization of One Member That Inhibits Pain*[J]. The Journal of Biological Chemistry, 2001, 19 1: 42639-42644. DOI:
10.1074/jbc.m107351200[2] DOUGLAS MCHUGH. Δ(9) -Tetrahydrocannabinol and N-arachidonyl glycine are full agonists at GPR18 receptors and induce migration in human endometrial HEC-1B cells.[J]. British Journal of Pharmacology, 2012: 2414-2424. DOI:
10.1111/j.1476-5381.2011.01497.x[3] DOUGLAS MCHUGH. siRNA knockdown of GPR18 receptors in BV-2 microglia attenuates N-arachidonoyl glycine-induced cell migration.[J]. Journal of Molecular Signaling, 2012, 7 1: 10. DOI:
10.1186/1750-2187-7-10[4] RINA TAKENOUCHI. N-arachidonoyl glycine induces macrophage apoptosis via GPR18[J]. Biochemical and biophysical research communications, 2012, 418 2: Pages 366-371. DOI:
10.1016/j.bbrc.2012.01.027[5] SUMNER H. BURSTEIN. Resolution of inflammation by N-arachidonoylglycine[J]. Journal of cellular biochemistry, 2011, 112 11: 3227-3233. DOI:
10.1002/jcb.23245[6] LINDA CONSOLE-BRAM . N-arachidonoyl glycine, another endogenous agonist of GPR55[J]. Biochemical and biophysical research communications, 2017, 490 4: Pages 1389-1393. DOI:
10.1016/j.bbrc.2017.07.038