ArticleNature communications2015
Structure and function of lysosomal phospholipase A2 and lecithin:cholesterol acyltransferase.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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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Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- LCAT acts as a molecular switch and regulates rooster sperm motility in vitro.Molecular & cellular proteomics : MCP · 2026Article
- Molecular insights into fungal inositol phosphorylceramide synthesis and its inhibition by antifungal aureobasidin A.Nature communications · 2026Article
- Broken Balance: Emerging Cross-Talk Between Proteostasis and Lipostasis in Neurodegenerative Diseases.Cells · 2025Review
- Hepatic lipid remodeling in cold exposure uncovers direct regulation of bis(monoacylglycero)phosphate lipids by phospholipase A2 group XV.Cell metabolism · 2025Article
- Lecithin:cholesterol acyltransferase binds a discontinuous binding site on adjacent apolipoprotein A-I belts in HDL.Journal of lipid research · 2025Article
- α/β Hydrolases: Toward Unraveling Entangled Classification.Proteins · 2025Article
- Cellular and organismal function of choline metabolism.Nature metabolism · 2025Review
- Gliflozins, sucrose and flavonoids are allosteric activators of lecithin-cholesterol acyltransferase.Scientific reports · 2024Article
- Activity-Based Acylome Profiling withJournal of the American Chemical Society · 2024Article
- Rescue of Familial Lecithin:Cholesterol Acyltranferase Deficiency Mutations with an Allosteric Activator.Molecular pharmacology · 2024Article
- The role of lysosomal phospholipase A2 in the catabolism of bis(monoacylglycerol)phosphate and association with phospholipidosis.Journal of lipid research · 2024Article
- Targeting host-specific metabolic pathways-opportunities and challenges for anti-infective therapy.Frontiers in molecular biosciences · 2024Review
- Familial LCAT Deficiency and Low HDL-C Levels: In silico Characterization of Two Rare LCAT Missense Mutations.The application of clinical genetics · 2024Article
- Cellular Export Fate of Liposomal Spherical Nucleic Acids.ACS nano · 2023Article
- Effect of Short-Chain Fatty Acids and Polyunsaturated Fatty Acids on Metabolites in H460 Lung Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- M05B5.4 (lysosomal phospholipase A2) promotes disintegration of autophagic vesicles to maintainAutophagy · 2022Article
- Genome-Wide CRISPR-Cas9 Screen Does Not Identify Host Factors Modulating Streptococcus agalactiae β-Hemolysin/Cytolysin-Induced Cell Death.Microbiology spectrum · 2022Article
- Acyl-CoA-dependent and acyl-CoA-independent avocado acyltransferases positively influence oleic acid content in nonseed triacylglycerols.Frontiers in plant science · 2022Article
- Influence of lecithin cholesterol acyltransferase alteration during different pathophysiologic conditions: A 45 years bibliometrics analysis.Frontiers in pharmacology · 2022Article
- Proteomic and lipidomic profiling of demyelinating lesions identifies fatty acids as modulators in lesion recovery.Cell reports · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Lysosomal phospholipase A2 (LPLA2) and lecithin:cholesterol acyltransferase (LCAT) belong to a structurally uncharacterized family of key lipid-metabolizing enzymes responsible for lung surfactant catabolism and for reverse cholesterol transport, respectively. Whereas LPLA2 is predicted to underlie the development of drug-induced phospholipidosis, somatic mutations in LCAT cause fish eye disease and familial LCAT deficiency. Here we describe several high-resolution crystal structures of human LPLA2 and a low-resolution structure of LCAT that confirms its close structural relationship to LPLA2. Insertions in the α/β hydrolase core of LPLA2 form domains that are responsible for membrane interaction and binding the acyl chains and head groups of phospholipid substrates. The LCAT structure suggests the molecular basis underlying human disease for most of the known LCAT missense mutations, and paves the way for rational development of new therapeutics to treat LCAT deficiency, atherosclerosis and acute coronary syndrome.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.