Hepatic PCSK9 expression is regulated by nutritional status via insulin and sterol regulatory element-binding protein 1c
Philippe Costet,Bertrand Cariou,Gilles Lambert,Florent Lalanne,Bernard Lardeux,Anne Laure Jarnoux,Aldo Grefhorst,Bart Staels,Michel Krempf +8 more
TL;DR: Results show that PCSK9 expression is regulated by nutritional status and insulinemia.
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About: This article is published in Journal of Biological Chemistry. The article was published on 10 Mar 2006. and is currently open access. The article focuses on the topics: Sterol regulatory element-binding protein & Apolipoprotein B.
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Citations
Nutrition and genetics in NAFLD : The perfect binomium
TL;DR: The premise of this review is to discuss the relevance of personalized nutritional advices as a novel therapeutic approach in NAFLD tailored management.
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Role of Insulin in the Regulation of Proprotein Convertase Subtilisin/Kexin Type 9
Ji Miao,Praveen V. Manthena,Mary E. Haas,Alisha V. Ling,Dong-Ju Shin,Mark J. Graham,Rosanne M. Crooke,Jingwen Liu,Sudha B. Biddinger +8 more
TL;DR: Data indicate that although insulin induces PCSK9 expression, it is not the sole or even dominant regulator ofPCSK9 under all conditions.
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Physiological and therapeutic regulation of PCSK9 activity in cardiovascular disease
TL;DR: The first outcome data of the PCSK9 inhibitor evolocumab reported a significant reduction in the composite endpoint (cardiovascular death, myocardial infarction, or stroke) and further outcome data are awaited.
Importance of Proprotein Convertase Subtilisin/Kexin Type 9 in the Hormonal and Dietary Regulation of Rat Liver Low-Density Lipoprotein Receptors
TL;DR: The identification of PCSK9 regulation by these various treatments is important in understanding of the physiological function of this protein and points to new targets for therapeutic treatments to increase hepatic LDLR numbers.
85
Endocytosis of lipoproteins.
TL;DR: During their metabolism, all lipoproteins undergo endocytosis, either to be degraded intracellularly, for example in hepatocytes or macrophages, or to be re-secreted, for instance in the course of transcytosis by endothelial cells.
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References
Role of LXRs in control of lipogenesis
Joshua R. Schultz,Hua Tu,Alvin Luk,Joyce J. Repa,Julio C. Medina,Leping Li,Susan Schwendner,Shelley Wang,Martin Thoolen,David J. Mangelsdorf,Kevin D. Lustig,Bei Shan +11 more
TL;DR: The identification here of a synthetic, nonsteroidal LXR-selective agonist series represented by T0314407 and T0901317 revealed a novel physiological role of LXR, and suggested that the increase in plasma lipids occurs via NXR-mediated induction of the sterol regulatory element-binding protein 1 (SREBP-1) lipogenic program.
Regulation of mouse sterol regulatory element-binding protein-1c gene (SREBP-1c) by oxysterol receptors, LXRα and LXRβ
Joyce J. Repa,Guosheng Liang,Jiafu Ou,Yuriy Bashmakov,Jean-Marc A. Lobaccaro,Iichiro Shimomura,Bei Shan,Michael S. Brown,Joseph L. Goldstein,David J. Mangelsdorf +9 more
TL;DR: A novel LXR target is described, the sterol regulatory element-binding protein-1c gene (SREBP-1C), which encodes a membrane-bound transcription factor of the basic helix-loop-helix-leucine zipper family and reveals a unique regulatory interplay between cholesterol and fatty acid metabolism.
Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes
Jay D. Horton,Nila Shah,Janet A. Warrington,Norma N. Anderson,Sahng Wook Park,Michael S. Brown,Joseph L. Goldstein +6 more
TL;DR: Through application of stringent combinatorial criteria, the transgenic/knockout approach allows identification of genes whose activities are likely to be controlled directly by one family of transcription factors, in this case the SREBPs.
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SREBP transcription factors: master regulators of lipid homeostasis.
TL;DR: The unique regulation and activation properties of each SREBP isoform facilitate the co-ordinate regulation of lipid metabolism; however, further studies are needed to understand the detailed regulation pathways that specifically regulate each S REBP isoforms.
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Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9.
Jonathan Cohen,Alexander Pertsemlidis,Ingrid K. Kotowski,Randall B. Graham,Christine Kim Garcia,Helen H. Hobbs +5 more
TL;DR: In this article, the coding region of PCSK9 was sequenced in 128 subjects (50% African American) with low plasma levels of LDL and found two nonsense mutations (Y142X and C679X) were common in African Americans (combined frequency, 2%) but rare in European Americans (< 0.1%).
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