Short CommunicationCloning, Expression, and Chromosomal Localization of Human Long-Chain Fatty Acid-CoA Ligase 4 (FACL4)☆
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Cited by (104)
Attenuated and delayed niacin skin flushing in schizophrenia and affective disorders: A potential clinical auxiliary diagnostic marker
2021, Schizophrenia ResearchCitation Excerpt :On the one hand, Horrobin and his colleagues hypothesized that the disturbance of membrane PUFA homeostasis may be the pathological mechanism of the cutaneous niacin bluntness due to the reduced reservoir of available membrane AA, as they observed a significant decrease of membrane AA and docosahexaenoic acid (DHA) in red blood cells of SZ patients(Glen et al., 1996). Subsequently, several biological mechanisms which can affect membrane PUFA homeostasis were reported to be associated with the niacin skin responses, such as the dissociation of AA mediated by PLA2 (Tavares et al., 2003; Xu et al., 2019; Yang et al., 2021), the incorporation of AA mediated by long-chain fatty acid-CoA ligase 4 (FACL4) (Cao et al., 1998; Covault et al., 2004), and the excessive oxidative stress which may cause a reduced level of membrane AA (Koga et al., 2016). Intriguingly, PUFA deficiency (Bazan, 2003; Bazinet and Laye, 2014) and increased oxidative stress (Maes et al., 2020) were also reported as biological etiologies of psychiatric disorders.
Long-chain acyl-CoA synthetase 4 participates in the formation of highly unsaturated fatty acid-containing phospholipids in murine macrophages
2019, Biochimica et Biophysica Acta - Molecular and Cell Biology of LipidsRole of acyl-CoA synthetase ACSL4 in arachidonic acid metabolism
2019, Prostaglandins and Other Lipid Mediators
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Sequence data from this article have been deposited with the GenBank Data Library under Accession No. AF030555.
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