Cholesterylester transfer protein
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| Cholesteryl ester transfer protein, plasma
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| PDB rendering based on 2obd. | |||||||||||
| Identifiers | |||||||||||
| Symbol(s) | CETP; | ||||||||||
| External IDs | OMIM: 118470 Homologene: 47904 | ||||||||||
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| RNA expression pattern | |||||||||||
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| Orthologs | |||||||||||
| Human | Mouse | ||||||||||
| Entrez | 1071 | na | |||||||||
| Ensembl | ENSG00000087237 | na | |||||||||
| Uniprot | P11597 | na | |||||||||
| Refseq | NM_000078 (mRNA) NP_000069 (protein) | na (mRNA) na (protein) | |||||||||
| Location | Chr 16: 55.55 - 55.58 Mb | na | |||||||||
| Pubmed search | [1] | na | |||||||||
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Cholesteryl ester transfer protein (CETP) (also called plasma lipid transfer protein) is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins. It collects triglycerides from very low density or low density lipoproteins (VLDL or LDL) and exchanges them for cholesteryl esters from high density lipoproteins (and vice versa). Most of the time, however, CETP does a homoexchange- trading a triglyceride for a triglyceride or a cholesteryl ester for a cholesteryl ester.
Genetics
The CETP gene is located on the sixteenth chromosome (16q21).
Role in disease
Rare mutations leading to increased function of CETP have been linked to accelerated atherosclerosis.[1] In contrast, a polymorphism (I405V) of the CETP gene leading to lower serum levels has also been linked to exceptional longevity.[1] However, this mutation also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia.[1] The D442G mutation, which lowers CETP levels and increases HDL levels also increases coronary heart disease.[1]
Elaidic acid—a major component of trans fat—increases CETP activity.[1]
Pharmacology
As HDL has a protective function in atherosclerosis and cardiovascular disease, and certain disease states (such as the metabolic syndrome) feature low HDL, pharmacological inhibition of CETP is being studied as a method to improve HDL levels.[1] Specifically, the small molecular agent torcetrapib was shown to increase HDL levels (alone and with a statin) and lower LDL (when co-administered with a statin) in a 2004 study.[1] Studies into cardiovascular endpoints, however, were largely disappointing; while they confirmed the change in lipid levels, most reported an increase in blood pressure, no change in atherosclerosis,[1][1] and (in a trial of a combination of torcetrapib and atorvastatin) an increase in cardiovascular events and mortality.[1]
A compound related to torcetrapib, going by the investigative name JTT-705/R1658, is undergoing studies.[1] It increases HDL levels by 30% (as compared to 60% by torcetrapib).[1]. Another CETP inhibitor under development is Merck's MK-0859 anacetrapib, which in initial studies has been shown not to increase blood pressure.[1]
References
Further reading
- Okajima F (2002). "[Distribution of sphingosine 1-phosphate in plasma lipoproteins and its role in the regulation of the vascular cell functions]". Tanpakushitsu Kakusan Koso 47 (4 Suppl): 480-7. PMID 11915346.
- Barter PJ, Brewer HB, Chapman MJ, et al. (2003). "Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis.". Arterioscler. Thromb. Vasc. Biol. 23 (2): 160-7. PMID 12588754.
- Dallinga-Thie GM, Dullaart RP, van Tol A (2007). "Concerted actions of cholesteryl ester transfer protein and phospholipid transfer protein in type 2 diabetes: effects of apolipoproteins.". Curr. Opin. Lipidol. 18 (3): 251-7. doi:10.1097/MOL.0b013e3280e12685. PMID 17495597.
External links
Protein: glycoproteins |
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| Activin - ADAM protein - Alpha 1-antichymotrypsin - Apolipoprotein H - CD70 - Asialoglycoprotein - Avidin - B-cell activating factor - 4-1BB ligand - Cholesterylester transfer protein - Clusterin - Colony-stimulating factor - Haemopexin - Inhibin - Lactoferrin - Membrane glycoproteins - Mucoprotein - Myelin protein zero - Osteonectin - Protein C - Protein S - Proteoglycan - Serum Amyloid P component - Sialoglycoprotein (CD43, Glycophorin, Glycophorin C) - Thrombopoietin - Thyroglobulin - Thyroxine-binding proteins - Transcortin - Tumor necrosis factor-alpha - Uteroglobin - Vitronectin |
Proteins: carrier proteins | |
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| Hormone | Follistatin - Growth hormone binding protein - Insulin-like growth factor binding protein - Neurophysins (Neurophysin I, II) Sex hormone binding globulin/Androgen binding protein - Transcortin - Thyroxine-binding globulin - Transthyretin |
| Metal/element | calcium (Calcium-binding protein, Calmodulin-binding proteins) - copper (Ceruloplasmin) - iron (Iron-binding proteins, Transferrin receptor) |
| Vitamin | Retinol binding protein (4) - Transcobalamin |
| Other | Acyl carrier protein - Adaptor protein - Cholesterylester transfer protein - F-box protein - GTP-binding protein - Latent TGF-beta binding protein - Light-harvesting complex - Membrane transport protein |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
