An anatomical and temporal portrait of physiological substrates for fatty acid amide hydrolase

Journal of Lipid Research

Volumn 52, Issue 2, 2011, Pages 337-344

  Long, Jonathan Z ^a   LaCava, Melanie ^a   Jin, Xin ^a   Cravatt, Benjamin F ^a  

^a SCRIPPS RESEARCH INSTITUTE   (United States)

Author keywords

Anandamide; Endocannabinoid; Metabolomics; Taurine

Indexed keywords

AMIDE; ANANDAMIDE; FATTY ACID AMIDASE; FATTY ACID AMIDASE INHIBITOR; N ACYL ETHANOLAMINE; N ACYL TAURINE; UNCLASSIFIED DRUG;

ANIMAL TISSUE; ARTICLE; BRAIN TISSUE; CONTROLLED STUDY; ENZYME SUBSTRATE; KIDNEY PARENCHYMA; LIPID METABOLISM; LIPOGENESIS; LIVER PARENCHYMA; MOUSE; NONHUMAN; PRIORITY JOURNAL; TESTIS;

EID: 78751514576     PISSN: 00222275     EISSN: 15397262     Source Type: Journal    
DOI: 10.1194/jlr.M012153     Document Type: Article

References (34)

1. Cravatt, B. F., D. K. Giang, S. P. Mayfield, D. L. Boger, R. A. Lerner, and N. B. Gilula. 1996. Molecular characterization of an enzyme that degrades neuromodulatory fatty-acid amides. Nature. 384: 83-87.
2. Simon, G. M., and B. F. Cravatt. 2010. Activity-based proteomics of enzyme superfamilies: serine hydrolases as a case study. J. Biol. Chem. 285: 11051-11055.
3. Ahn, K., M. K. McKinney, and B. F. Cravatt. 2008. Enzymatic pathways that regulate endocannabinoid signaling in the nervous system. Chem. Rev. 108: 1687-1707.
4. Naidu, P. S., S. G. Kinsey, T. L. Guo, B. F. Cravatt, and A. H. Lichtman. 2010. Regulation of inflammatory pain by inhibition of fatty acid amide hydrolase. J. Pharmacol. Exp. Ther. 334: 182-190.
5. Kinsey, S. G., J. Z. Long, S. T. O'Neal, R. A. Abdullah, J. L. Poklis, D. L. Boger, B. F. Cravatt, and A. H. Lichtman. 2009. Blockade of endocannabinoid-degrading enzymes attenuates neuropathic pain. J. Pharmacol. Exp. Ther. 330: 902-910.
6. Cravatt, B. F., K. Demarest, M. P. Patricelli, M. H. Bracey, D. K. Giang, B. R. Martin, and A. H. Lichtman. 2001. Supersensitivity to anandamide and enhanced endogenous cannabinoid signaling in mice lacking fatty acid amide hydrolase. Proc. Natl. Acad. Sci. USA. 98: 9371-9376.
7. Matsuda, L. A., S. J. Lolait, M. J. Brownstein, A. C. Young, and T. I. Bonner. 1990. Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Nature. 346: 561-564.
8. Kathuria, S., S. Gaetani, D. Fegley, F. Valino, A. Duranti, A. Tontini, M. Mor, G. Tarzia, G. La Rana, A. Calignano, et al. 2003. Modulation of anxiety through blockade of anandamide hydrolysis. Nat. Med. 9: 76-81.
9. Naidu, P. S., S. A. Varvel, K. Ahn, B. F. Cravatt, B. R. Martin, and A. H. Lichtman. 2007. Evaluation of fatty acid amide hydrolase inhibition in murine models of emotionality. Psychopharmacology (Berl.). 192: 61-70.
10. Bambico, F. R., and G. Gobbi. 2008. The cannabinoid CB1 receptor and the endocannabinoid anandamide: possible antidepressant targets. Expert Opin. Ther. Targets. 12: 1347-1366.
11. Boger, D. L., H. Miyauchi, W. Du, C. Hardouin, R. A. Fecik, H. Cheng, I. Hwang, M. P. Hedrick, D. Leung, O. Acevedo, et al. 2005. Discovery of a potent, selective, and efficacious class of reversible alpha-ketoheterocycle inhibitors of fatty acid amide hydrolase effective as analgesics. J. Med. Chem. 48: 1849-1856.
12. Cravatt, B. F., A. Saghatelian, E. G. Hawkins, A. B. Clement, M. H. Bracey, and A. H. Lichtman. 2004. Functional disassociation of the central and peripheral fatty acid amide signaling systems. Proc. Natl. Acad. Sci. USA. 101: 10821-10826.
13. Mackie, K. 2006. Cannabinoid receptors as therapeutic targets. Annu. Rev. Pharmacol. Toxicol. 46: 101-122.
14. Ahn, K., D. S. Johnson, and B. F. Cravatt. 2009. Fatty acid amide hydrolase as a potential therapeutic target for the treatment of pain and CNS disorders. Expert Opin Drug Discov. 4: 763-784.
15. Sagar, D. R., D. A. Kendall, and V. Chapman. 2008. Inhibition of fatty acid amide hydrolase produces PPAR-alpha-mediated analgesia in a rat model of inflammatory pain. Br. J. Pharmacol. 155: 1297-1306.
16. Maione, S., T. Bisogno, V. de Novellis, E. Palazzo, L. Cristino, M. Valenti, S. Petrosino, V. Guglielmotti, F. Rossi, and V. Di Marzo. 2006. Elevation of endocannabinoid levels in the ventrolateral periaqueductal grey through inhibition of fatty acid amide hydrolase affects descending nociceptive pathways via both cannabinoid receptor type 1 and transient receptor potential vanilloid type-1 receptors. J. Pharmacol. Exp. Ther. 316: 969-982.
17. Saghatelian, A., S. A. Trauger, E. J. Want, E. G. Hawkins, G. Siuzdak, and B. F. Cravatt. 2004. Assignment of endogenous substrates to enzymes by global metabolite profiling. Biochemistry. 43: 14332-14339.
18. Saghatelian, A., M. K. McKinney, M. Bandell, A. Patapoutian, and B. F. Cravatt. 2006. A FAAH-regulated class of N-acyl taurines that activates TRP ion channels. Biochemistry. 45: 9007-9015.
19. Ahn, K., D. S. Johnson, M. Mileni, D. Beidler, J. Z. Long, M. K. McKinney, E. Weerapana, N. Sadagopan, M. Liimatta, S. E. Smith, et al. 2009. Discovery and characterization of a highly selective FAAH inhibitor that reduces inflammatory pain. Chem. Biol. 16: 411-420.
20. Liu, Y., M. P. Patricelli, and B. F. Cravatt. 1999. Activity-based protein profiling: the serine hydrolases. Proc. Natl. Acad. Sci. USA. 96: 14694-14699.
21. Patricelli, M. P., D. K. Giang, L. M. Stamp, and J. J. Burbaum. 2001. Direct visualization of serine hydrolase activities in complex proteomes using fluorescent active site-directed probes. Proteomics. 1: 1067-1071.
22. Li, W., J. L. Blankman, and B. F. Cravatt. 2007. A functional proteomic strategy to discover inhibitors for uncharacterized hydrolases. J. Am. Chem. Soc. 129: 9594-9595.
23. Leung, D., C. Hardouin, D. L. Boger, and B. F. Cravatt. 2003. Discovering potent and selective reversible inhibitors of enzymes in complex proteomes. Nat. Biotechnol. 21: 687-691.
24. Fegley, D., S. Gaetani, A. Duranti, A. Tontini, M. Mor, G. Tarzia, and D. Piomelli. 2005. Characterization of the fatty acid amide hydrolase inhibitor cyclohexyl carbamic acid 3′-carbamoyl-biphenyl-3-yl ester (URB597): effects on anandamide and oleoylethanolamide deactivation. J. Pharmacol. Exp. Ther. 313: 352-358.
25. Kilaru, A., G. Isaac, P. Tamura, D. Baxter, S. R. Duncan, B. J. Venables, R. Welti, P. Koulen, and K. D. Chapman. 2010. Lipid profiling reveals tissue-specific differences for ethanolamide lipids in mice lacking fatty acid amide hydrolase. Lipids. 45: 863-875.
26. Leung, D., A. Saghatelian, G. M. Simon, and B. F. Cravatt. 2006. Inactivation of N-acyl phosphatidylethanolamine phospholipase D reveals multiple mechanisms for the biosynthesis of endocannabinoids. Biochemistry. 45: 4720-4726.
27. Ueda, N., Y. Okamoto, and J. Morishita. 2005. N- acylphosphatidylethanolamine-hydrolyzing phospholipase D: a novel enzyme of the beta-lactamase fold family releasing anandamide and other N-acylethanolamines. Life Sci. 77: 1750-1758. (Pubitemid 41073668)
28. Reilly, S. J., E. M. O'Shea, U. Andersson, J. O'Byrne, S. E. Alexson, and M. C. Hunt. 2007. A peroxisomal acyltransferase in mouse identifies a novel pathway for taurine conjugation of fatty acids. FASEB J. 21: 99-107.
29. Rosendal, J., and J. Knudsen. 1992. A fast and versatile method for extraction and quantitation of long-chain acyl-CoA esters from tissue: content of individual long-chain acyl-CoA esters in various tissues from fed rat. Anal. Biochem. 207: 63-67.
30. Golovko, M. Y., and E. J. Murphy. 2004. An improved method for tissue long-chain acyl-CoA extraction and analysis. J. Lipid Res. 45: 1777-1782.
31. Ohlsson, C., S. Mohan, K. Sjogren, A. Tivesten, J. Isgaard, O. Isaksson, J. O. Jansson, and J. Svensson. 2009. The role of liver-derived insulin-like growth factor-I. Endocr. Rev. 30: 494-535.
32. Qian, S., F. Fu, W. Li, Q. Chen, and F. J. de Sauvage. 1998. Primary role of the liver in thrombopoietin production shown by tissuespecific knockout. Blood. 92: 2189-2191. (Pubitemid 28446716)
33. Kuter, D. J., and C. G. Begley. 2002. Recombinant human thrombopoietin: basic biology and evaluation of clinical studies. Blood. 100: 3457-3469.
34. Trauner, M., and J. L. Boyer. 2003. Bile salt transporters: molecular characterization, function, and regulation. Physiol. Rev. 83: 633-671.