CETP Activity Assay Kit, mammalian
- Known as:
- CETP Activity Assay Kit, mammalian
- Catalog number:
- kt-149
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- CETP Activity Assay Kit mammalian
Related genes to: CETP Activity Assay Kit, mammalian
- Gene:
- CETP NIH gene
- Name:
- cholesteryl ester transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFF
- Chromosome:
- 16q13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-17
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- Cholesteryl ester transfer protein (CETP), a key drug target in cardiovascular disease, primarily regulates plasma circulating levels of lipids (within high, low, and very-low-density lipoproteins). In addition to its terminal openings, CETP has 2 additional openings, plugged by a phospholipid (PL) each. However, the mechanism, by which CETP moves lipids between lipoproteins, and roles of PL plugs in CETP function remain elusive. Further, small-molecule inhibitors targeting CETP tunnel displace PL during CETP inhibition. Here, using steered molecular dynamics simulations followed by mutagenesis, we show that CETP-bound PLs are indispensable in establishing the optimal architecture of CETP tunnel. PLs were critical in synchronizing domain movements of CETP while accelerating triglyceride traversal through the tunnel and their activity regulated through salt bridge interactions. Most notably, PLs bound within the CETP tunnel accelerated lipid movement through a novel "gliding" mechanism, in which a bound PL directly facilitates the movement of a second lipid species. Structural and functional analyses revealed that lipid traversal through the central tunnel of CETP was facilitated through hydrophobic-interaction-mediated diffusion. Further, conserved phenylalanine flaps regulated lipid movement by concerted opening and closing to prevent lipid backflow in the absence of an active motor. This study provides in-depth understanding of the mechanism of lipid exchange by CETP, guided and accentuated by its interaction with PLs. The conserved nature of these critical structural elements suggests that this mechanism may extend to other members of this family, expanding our understanding of lipid transport in this clinically important protein class. - Source: PubMed
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Meng QiZhou ZihaoZhang Wanchao - LDL cholesterol (LDL-C) is the central causal factor for atherosclerotic cardiovascular disease (ASCVD), and its reduction is a cornerstone of both primary and secondary prevention. Since the introduction of statins more than three decades ago, LDL-C-lowering therapy has expanded substantially, now encompassing ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9)-targeting agents, bempedoic acid, and other emerging modalities. This expanding therapeutic landscape has improved the feasibility of achieving guideline-recommended LDL-C targets, but it has also increased the complexity of clinical decision making. This review provides a contemporary and practical overview of the LDL-C-lowering strategies, beginning with the initial evaluation of patients with elevated LDL-C, including differentiation between primary and secondary causes and the identification of familial hypercholesterolemia (FH). We summarize the current treatment targets for primary and secondary prevention, highlight the optimal selection and use of statins, and discuss the assessment and management of statin intolerance, including the role of the nocebo effect. Non-statin therapies, including ezetimibe, bile acid sequestrants, PCSK9 inhibitors, inclisiran, and bempedoic acid, are reviewed with an emphasis on their mechanisms, efficacy, and clinical positioning. Advanced therapies for severe dyslipidemia, such as lipoprotein apheresis, lomitapide, and evinacumab, are also discussed in this review. Finally, we outline the future directions, including oral PCSK9 inhibitors, next-generation cholesteryl ester transfer protein (CETP) inhibitors, lipoprotein(a)-lowering agents, and genome-editing approaches. Collectively, these developments offer new opportunities to address unmet clinical needs, particularly in patients with FH, statin intolerance, and residual cardiovascular risk. A comprehensive understanding of these therapies is essential for further reducing the burden of ASCVD in the coming decades. - Source: PubMed
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