ArticleMolecular biology of the cell2005
Triacylglycerol hydrolase is localized to the endoplasmic reticulum by an unusual retrieval sequence where it participates in VLDL assembly without utilizing VLDL lipids as substrates.
Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 80 citations in OpenAlex.
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- Single-Cell and Subcellular Analysis Using Ultrahigh Resolution 21 T MALDI FTICR Mass Spectrometry.Analytical chemistry · 2023Article
- Carboxylesterase 1 family knockout alters drug disposition and lipid metabolism.Acta pharmaceutica Sinica. B · 2023Article
- Adipose tissue-specific ablation of Ces1d causes metabolic dysregulation in mice.Life science alliance · 2022Article
- The Biological Functions and Regulatory Mechanisms of Fatty Acid Binding Protein 5 in Various Diseases.Frontiers in cell and developmental biology · 2022Review
- Lipolysis: cellular mechanisms for lipid mobilization from fat stores.Nature metabolism · 2021Review
- Carnitine palmitoyltransferase 1C negatively regulates the endocannabinoid hydrolase ABHD6 in mice, depending on nutritional status.British journal of pharmacology · 2021Article
- Nuclear-lipid-droplet proteome: carboxylesterase as a nuclear lipase involved in lipid-droplet homeostasis.Heliyon · 2021Article
- From physics to physiology at the membrane-motor interface.Nature reviews. Molecular cell biology · 2020Article
- The cell biology of the hepatocyte: A membrane trafficking machine.The Journal of cell biology · 2019Review
- Ces1d deficiency protects against high-sucrose diet-induced hepatic triacylglycerol accumulation.Journal of lipid research · 2019Article
- Characterization of Endocannabinoid-Metabolizing Enzymes in Human Peripheral Blood Mononuclear Cells under Inflammatory Conditions.Molecules (Basel, Switzerland) · 2018Article
- Carboxylesterases in lipid metabolism: from mouse to human.Protein & cell · 2018Review
- Kinesin-dependent mechanism for controlling triglyceride secretion from the liver.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Complex role of autophagy in regulation of hepatic lipid and lipoprotein metabolism.Journal of biomedical research · 2017Article
- Structure, Function and Metabolism of Hepatic and Adipose Tissue Lipid Droplets: Implications in Alcoholic Liver Disease.Current molecular pharmacology · 2017Review
- Sodium sulfite promotes the assembly and secretion of very low-density lipoprotein in HL-7702 hepatocytes.Toxicology reports · 2016Article
- Hepatic fatty acid trafficking: multiple forks in the road.Advances in nutrition (Bethesda, Md.) · 2013Review
- Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) deficiencies affect expression of lipolytic activities in mouse adipose tissues.Molecular & cellular proteomics : MCP · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of hepatic intracellular triacylglycerol (TG) is mobilized by lipolysis followed by reesterification to reassemble TG before incorporation into a very-low-density lipoprotein (VLDL) particle. Triacylglycerol hydrolase (TGH) is a lipase that hydrolyzes TG within hepatocytes. Immunogold electron microscopy in transfected cells revealed a disparate distribution of this enzyme within the endoplasmic reticulum (ER), with particularly intense localization in regions surrounding mitochondria. TGH is localized to the lumen of the ER by the C-terminal tetrapeptide sequence HIEL functioning as an ER retention signal. Deletion of HIEL resulted in secretion of catalytically active TGH. Mutation of HIEL to KDEL, which is the consensus ER retrieval sequence in animal cells, also resulted in ER retention and conservation of lipolytic activity. However, KDEL-TGH was not as efficient at mobilizing lipids for VLDL secretion and exhibited an altered distribution within the ER. TGH is a glycoprotein, but glycosylation is not required for catalytic activity. TGH does not hydrolyze apolipoprotein B-associated lipids. This suggests a mechanism for vectored movement of TGs onto developing VLDL in the ER as TGH may mobilize TG for VLDL assembly, but will not access this lipid once it is associated with VLDL.
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