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. 2024 Jan 12;23:14. doi: 10.1186/s12944-023-01993-y

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Biogenesis, lipidation and intracellular trafficking of VLDL. The assembly of VLDL in the liver begins with the cotranslational translation of apolipoprotein B (APOB) across the rough endoplasmic reticulum (RER) membrane. Microsomal triglyceride transfer protein (MTP) plays an essential role in the initial lipidation of APOB by extracting phospholipids and triglycerides (TGs) from the endoplasmic reticulum (ER). Without sufficient lipidation, nascent APOB is degraded. After the initial lipidation, VLDL is further lipidated with a large amount of lipids to form mature VLDL. To exit the endoplasmic reticulum, VLDL is packaged into transport vesicles called coat protein complex II (COPII), which is initiated by the activation of the small Ras-like GTPase SAR1.