ArticleThe Journal of biological chemistry2015
Angiopoietin-like 4 Modifies the Interactions between Lipoprotein Lipase and Its Endothelial Cell Transporter GPIHBP1.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Protein-coding variants implicate novel genes related to lipid homeostasis contributing to body-fat distribution.Nature genetics · 2019Pooled it
- Angiopoietin-like 3 monomers are abundant in human plasma but are unable to inhibit endothelial lipase.JCI insight · 2025Article
- Secretion and transfer of adipose lipoprotein lipase utilizes neutral sphingomyelinase 2 generated exosomes.bioRxiv : the preprint server for biology · 2025Article
- ANGPTL4: A Comprehensive Review of 25 Years of Research.Cancers · 2025Review
- Comprehensive profiling of chemokine and NETosis-associated genes in sarcopenia: construction of a machine learning-based diagnostic nomogram.Frontiers in medicine · 2025Article
- Exercise-Induced cytokines, diet, and inflammation and their role in adipose tissue metabolism.Health science reports · 2024Review
- ANGPTL4 Suppresses Clear Cell Renal Cell Carcinoma via Inhibition of Lysosomal Acid Lipase.Cancer research communications · 2024Article
- A unified model for regulating lipoprotein lipase activity.Trends in endocrinology and metabolism: TEM · 2024Review
- Endothelial lipase variant T111I does not alter inhibition by angiopoietin-like proteins.Scientific reports · 2024Article
- Hypertriglyceridemia in Apoa5-/- mice results from reduced amounts of lipoprotein lipase in the capillary lumen.The Journal of clinical investigation · 2023Article
- Angiopoietin-like proteins inhibitors: New horizons in the treatment of atherogenic dyslipidemia and familial hypercholesterolemia.Cardiology journal · 2023Article
- Genetics of Cholesterol-Related Genes in Metabolic Syndrome: A Review of Current Evidence.Biomedicines · 2022Review
- An updated ANGPTL3-4-8 model as a mechanism of triglyceride partitioning between fat and oxidative tissues.Progress in lipid research · 2022Review
- Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8.American journal of physiology. Endocrinology and metabolism · 2021Review
- The Importance of Lipoprotein Lipase Regulation in Atherosclerosis.Biomedicines · 2021Review
- Regulation of plasma triglyceride partitioning by adipose-derived ANGPTL4 in mice.Scientific reports · 2021Article
- The intrinsic instability of the hydrolase domain of lipoprotein lipase facilitates its inactivation by ANGPTL4-catalyzed unfolding.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Lipoprotein Lipase and Its Regulators: An Unfolding Story.Trends in endocrinology and metabolism: TEM · 2021Review
- GPIHBP1 and ANGPTL4 Utilize Protein Disorder to Orchestrate Order in Plasma Triglyceride Metabolism and Regulate Compartmentalization of LPL Activity.Frontiers in cell and developmental biology · 2021Review
- ANGPTL4: a multifunctional protein involved in metabolism and vascular homeostasis.Current opinion in hematology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The release of fatty acids from plasma triglycerides for tissue uptake is critically dependent on the enzyme lipoprotein lipase (LPL). Hydrolysis of plasma triglycerides by LPL can be disrupted by the protein angiopoietin-like 4 (ANGPTL4), and ANGPTL4 has been shown to inactivate LPL in vitro. However, in vivo LPL is often complexed to glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1 (GPIHBP1) on the surface of capillary endothelial cells. GPIHBP1 is responsible for trafficking LPL across capillary endothelial cells and anchors LPL to the capillary wall during lipolysis. How ANGPTL4 interacts with LPL in this context is not known. In this study, we investigated the interactions of ANGPTL4 with LPL-GPIHBP1 complexes on the surface of endothelial cells. We show that ANGPTL4 was capable of binding and inactivating LPL complexed to GPIHBP1 on the surface of endothelial cells. Once inactivated, LPL dissociated from GPIHBP1. We also show that ANGPTL4-inactivated LPL was incapable of binding GPIHBP1. ANGPTL4 was capable of binding, but not inactivating, LPL at 4 °C, suggesting that binding alone was not sufficient for ANGPTL4's inhibitory activity. We observed that although the N-terminal coiled-coil domain of ANGPTL4 by itself and full-length ANGPTL4 both bound with similar affinities to LPL, the N-terminal fragment was more potent in inactivating both free and GPIHBP1-bound LPL. These results led us to conclude that ANGPTL4 can both bind and inactivate LPL complexed to GPIHBP1 and that inactivation of LPL by ANGPTL4 greatly reduces the affinity of LPL for GPIHBP1.
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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.