ArticleArteriosclerosis, thrombosis, and vascular biology2014
A regulator of secretory vesicle size, Kelch-like protein 12, facilitates the secretion of apolipoprotein B100 and very-low-density lipoproteins--brief report.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Intestinal KLHL12 is dispensable for lipid absorption and chylomicron metabolism.American journal of physiology. Endocrinology and metabolism · 2025Article
- Article
- VLDL Biogenesis and Secretion: It Takes a Village.Circulation research · 2024Review
- Cargo Receptor-Mediated ER Export in Lipoprotein Secretion and Lipid Homeostasis.Cold Spring Harbor perspectives in biology · 2023Review
- Surf4, cargo trafficking, lipid metabolism, and therapeutic implications.Journal of molecular cell biology · 2023Review
- Hsp40s play distinct roles during the initial stages of apolipoprotein B biogenesis.Molecular biology of the cell · 2022Article
- Metabolic-associated fatty liver disease and lipoprotein metabolism.Molecular metabolism · 2021Review
- Reticulon 3 regulates very low density lipoprotein secretion by controlling very low density lipoprotein transport vesicle biogenesis.Canadian journal of physiology and pharmacology · 2018Article
- Can modulators of apolipoproteinB biogenesis serve as an alternate target for cholesterol-lowering drugs?Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Review
- Hepatitis C Virus Lipoviroparticles Assemble in the Endoplasmic Reticulum (ER) and Bud off from the ER to the Golgi Compartment in COPII Vesicles.Journal of virology · 2017Article
- Hepatic Tm6sf2 overexpression affects cellular ApoB-trafficking, plasma lipid levels, hepatic steatosis and atherosclerosis.Human molecular genetics · 2017Article
- Endoplasmic Reticulum-Associated Degradation and Lipid Homeostasis.Annual review of nutrition · 2016Review
- Silencing of Small Valosin-containing Protein-interacting Protein (SVIP) Reduces Very Low Density Lipoprotein (VLDL) Secretion from Rat Hepatocytes by Disrupting Its Endoplasmic Reticulum (ER)-to-Golgi Trafficking.The Journal of biological chemistry · 2016Article
- Studying lipoprotein trafficking in zebrafish, the case of chylomicron retention disease.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Cholesterol and lipoprotein metabolism: Early Career Committee contribution.Arteriosclerosis, thrombosis, and vascular biology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveOne of the major risk factors for atherosclerosis is the plasma level of low-density lipoprotein (LDL), which is a product of very-low-density lipoprotein (VLDL). Hepatic apolipoprotein B100 (apoB100) is the essential component that provides structural stability to VLDL particles. Newly translated apoB100 is partially lipidated in the endoplasmic reticulum (ER), forming nascent apoB100-VLDL particles. These particles are further modified to form fully mature VLDLs in the Golgi apparatus. Therefore, the transport of nascent VLDL from the ER to the Golgi represents a critical step during VLDL maturation and secretion and in regulating serum LDL cholesterol levels. Our previous studies showed that apoB100 exits the ER in coat complex II vesicles (COPII), but the cohort of related factors that control trafficking is poorly defined. APPROACH AND
resultsExpression levels of Kelch-like protein 12 (KLHL12), an adaptor protein known to assist COPII-dependent transport of procollagen, were manipulated by using a KLHL12-specific small interfering RNA and a KLHL12 expression plasmid in the rat hepatoma cell line, McArdle RH7777. KLHL12 knockdown decreased the secreted and intracellular pools of apoB100, an effect that was attenuated in the presence of an autophagy inhibitor. KLHL12 knockdown also significantly reduced secretion of the most lipidated apoB100-VLDL species and led to the accumulation of apoB100 in the ER. Consistent with these data, KLHL12 overexpression increased apoB100 recovery and apoB100-VLDL secretion. Images obtained from confocal microscopy revealed colocalization of apoB100 and KLHL12, further supporting a direct link between KLHL12 function and VLDL trafficking from the ER.
conclusionsKLHL12 plays a critical role in facilitating the ER exit and secretion of apoB100-VLDL particles, suggesting that KLHL12 modulation would influence plasma lipid levels.
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Registered trials
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.