8erc

Structural highlights

Disease

MBOA7_HUMAN Autosomal recessive non-syndromic intellectual disability. The disease is caused by variants affecting the gene represented in this entry.

Function

MBOA7_HUMAN Acyltransferase which catalyzes the transfer of an acyl group from an acyl-CoA to a lysophosphatidylinositol (1-acylglycerophosphatidylinositol or LPI) leading to the production of a phosphatidylinositol (1,2-diacyl-sn-glycero-3-phosphoinositol or PI) and participates in the reacylation step of the phospholipid remodeling pathway also known as the Lands cycle (PubMed:18094042, PubMed:18772128). Prefers arachidonoyl-CoA as the acyl donor, thus contributing to the regulation of free levels arachidonic acid in cell (PubMed:18094042, PubMed:18772128). In liver, participates in the regulation of triglyceride metabolism through the phosphatidylinositol acyl-chain remodeling regulation (PubMed:32253259).^{[1] [2] [3]}

References

1. ↑ Lee HC, Inoue T, Imae R, Kono N, Shirae S, Matsuda S, Gengyo-Ando K, Mitani S, Arai H. Caenorhabditis elegans mboa-7, a member of the MBOAT family, is required for selective incorporation of polyunsaturated fatty acids into phosphatidylinositol. Mol Biol Cell. 2008 Mar;19(3):1174-84. PMID:18094042 doi:10.1091/mbc.e07-09-0893
2. ↑ Gijón MA, Riekhof WR, Zarini S, Murphy RC, Voelker DR. Lysophospholipid acyltransferases and arachidonate recycling in human neutrophils. J Biol Chem. 2008 Oct 31;283(44):30235-45. PMID:18772128 doi:10.1074/jbc.M806194200
3. ↑ Tanaka Y, Shimanaka Y, Caddeo A, Kubo T, Mao Y, Kubota T, Kubota N, Yamauchi T, Mancina RM, Baselli G, Luukkonen P, Pihlajamäki J, Yki-Järvinen H, Valenti L, Arai H, Romeo S, Kono N. LPIAT1/MBOAT7 depletion increases triglyceride synthesis fueled by high phosphatidylinositol turnover. Gut. 2021 Jan;70(1):180-193. PMID:32253259 doi:10.1136/gutjnl-2020-320646