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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/10/31 12:37:07」(JST)

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Apolipoprotein E (ApoE) is a class of apolipoprotein found in the chylomicron and Intermediate-density lipoprotein (IDLs) that is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.^[1] In peripheral tissues, ApoE is primarily produced by the liver and macrophages, and mediates cholesterol metabolism in an isoform-dependent manner. In the central nervous system, ApoE is mainly produced by astrocytes, and transports cholesterol to neurons via ApoE receptors, which are members of the low density lipoprotein receptor gene family.

Function

APOE ^[2] is 299 amino acids long and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood. It is synthesized principally in the liver, but has also been found in other tissues such as the brain, kidneys, and spleen. In the nervous system, non-neuronal cell types, most notably astroglia and microglia, are the primary producers of APOE, while neurons preferentially express the receptors for APOE. There are seven currently identified mammalian receptors for APOE which belong to the evolutionarily conserved low density lipoprotein receptor gene family.

APOE was initially recognized for its importance in lipoprotein metabolism and cardiovascular disease. Defects in APOE result in familial dysbetalipoproteinemia aka type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron, VLDL and LDL remnants^{[citation needed]}. More recently, it has been studied for its role in several biological processes not directly related to lipoprotein transport, including Alzheimer's disease (AD), immunoregulation, and cognition.

In the field of immune regulation, a growing number of studies point to APOE's interaction with many immunological processes, including suppressing T cell proliferation, macrophage functioning regulation, lipid antigen presentation facilitation (by CD1) ^[3] to natural killer T cell as well as modulation of inflammation and oxidation.^[4]

Gene

The gene, ApoE, is mapped to chromosome 19 in a cluster with Apolipoprotein C1 and the Apolipoprotein C2. The APOE gene consists of four exons and three introns, totaling 3597 base pairs. ApoE is transcriptionally activated by the liver X receptor (an important regulator of cholesterol, fatty acid, and glucose homeostasis) and peroxisome proliferator-activated receptor γ, nuclear receptors that form heterodimers with Retinoid X receptors.^[5] In melanocytic cells APOE gene expression may be regulated by MITF.^[6]

Polymorphisms

ApoE is polymorphic,^[7]^[8] with three major alleles: ApoE2 (cys112, cys158), ApoE3 (cys112, arg158), and ApoE4 (arg112, arg158).^[9] Although these allelic forms differ from each other by only one or two amino acids at positions 112 and 158,^[10]^[11]^[12] these differences alter apoE structure and function. These have physiological consequences:

E2 (rs7412) has an allele frequency of approximately 7 percent.^[13] This variant of the apoprotein binds poorly to cell surface receptors while E3 and E4 bind well.^[14] E2 is associated with both increased and decreased risk for atherosclerosis. Individuals with an E2/E2 combination may clear dietary fat slowly and be at greater risk for early vascular disease and the genetic disorder type III hyperlipoproteinemia—94.4% of such patients are E2/E2, while only ∼2% of E2/E2 develop the disease, so other environmental and genetic factors are likely to be involved (such as cholesterol in the diet and age).^[15]^[16]^[17] E2 has also been implicated in Parkinson's disease.^[18] E2 is no longer associated with Parkinson disease in a larger population association study.^[19]
E3 (rs429358) has an allele frequency of approximately 79 percent.^[13] It is considered the "neutral" Apo E genotype.
E4 has an allele frequency of approximately 14 percent.^[13] E4 has been implicated in atherosclerosis,^[20] Alzheimer's disease,^[21]^[22] impaired cognitive function,^[23]^[24] reduced hippocampal volume,^[24] HIV,^[25] faster disease progression in multiple sclerosis,^[26]^[27] unfavorable outcome after traumatic brain injury,^[28] ischemic cerebrovascular disease,^[29] sleep apnea,^[30]^[31] accelerated telomere shortening ^[32] and reduced neurite outgrowth.^[33] A notable advantage of the E4 allele (relative to E2 and E3) is a positive association with higher levels of vitamin D, which may help explain its prevalence despite its seeming complicity in various diseases or disorders.^[34]

However, there is much to be learned about these APOE isoforms, including the interaction of other potentially protective genetic polymorphisms, so caution is advised before making determinant statements about the influence of APOE polymorphisms; this is particularly true as it relates to how APOE isoforms influence cognition and the development of Alzheimers Disease. In addition, there is no evidence that APOE polymorphisms influence cognition in younger age groups (other than possible increased episodic memory ability and neural efficiency in younger APOE4 age groups), nor is there evidence that the APOE4 isoform places individuals at increased risk for any infectious disease.^{[citation needed]}

Alzheimer disease

The E4 variant is the largest known genetic risk factor for late-onset sporadic Alzheimer disease (AD) in a variety of ethnic groups.^[35] Caucasian and Japanese carriers of 2 E4 alleles have between 10 and 30 times the risk of developing AD by 75 years of age, as compared to those not carrying any E4 alleles. While the exact mechanism of how E4 causes such dramatic effects remains to be fully determined, evidence has been presented suggesting an interaction with amyloid.^[36] Alzheimer disease is characterized by build-ups of aggregates of the peptide beta-amyloid. Apolipoprotein E enhances proteolytic break-down of this peptide, both within and between cells. The isoform ApoE-ε4 is not as effective as the others at catalyzing these reactions, resulting in increased vulnerability to AD in individuals with that gene variation.^[37]

The pivotal role of ApoE in AD was first identified through linkage analysis by Margaret Pericak-Vance^[38] while working in the Roses lab at Duke University^[39] Linkage studies were followed by association analysis confirming the role of the ApoE4 allele as a strong genetic risk factor for AD.^[21]^[22]

Although 40-65% of AD patients have at least one copy of the ε4 allele, ApoE4 is not a determinant of the disease - at least a third of patients with AD are ApoE4 negative and some ApoE4 homozygotes never develop the disease. Yet those with two ε4 alleles have up to 20 times the risk of developing AD.^[40] There is also evidence that the ApoE2 allele may serve a protective role in AD.^[41] Thus, the genotype most at risk for Alzheimer disease and at an earlier age is ApoE 4,4. The ApoE 3,4 genotype is at increased risk, though not to the degree that those homozygous for ApoE 4 are. The genotype ApoE 3,3 is considered at normal risk for Alzheimer disease. The genotype ApoE 2,3 is considered at lower risk for Alzheimer disease. Interestingly, people with both a copy of the 2 allele and the 4 allele, ApoE 2,4, are at normal risk, similar to the ApoE 3,3 genotype.

Allele	ε2	ε3	ε4
Estimated worldwide human allele frequencies of ApoE * in Caucasian population^[42]
General Frequency	8.4%	77.9%	13.7%
AD Frequency	3.9%	59.4%	36.7%

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. ^{[§ 1]}

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Statin Pathway edit

^ The interactive pathway map can be edited at WikiPathways: "Statin_Pathway_WP430".

References

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^ ^a ^b ^c "Alzheimer Research Forum: Meta-Analyses of apolipoprotein E AD Association Studies".
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^ Federoff M, Jimenez-Rolando B, Nalls MA, Singleton AB (2012). "A large study reveals no association between APOE and Parkinson's disease.". Neurobiol Dis. 46 (2): 389–92. doi:10.1016/j.nbd.2012.02.002. PMID 22349451.
^ Mahley RW (April 1988). "Apolipoprotein E: cholesterol transport protein with expanding role in cell biology". Science 240 (4852): 622–30. doi:10.1126/science.3283935. PMID 3283935.
^ ^a ^b Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, Roses AD, Haines JL, Pericak-Vance MA (1993). "Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families". Science 261 (5123): 921–3. doi:10.1126/science.8346443. PMID 8346443.
^ ^a ^b Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS, Roses AD (1993). "Apolipoprotein E: High avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease". Proceedings of the National Academy of Sciences of the United States of America 90 (5): 1977–1981. doi:10.1073/pnas.90.5.1977. PMC 46003. PMID 8446617.
^ Deary IJ, Whiteman MC, Pattie A, Starr JM, Hayward C, Wright AF, Carothers A, Whalley LJ (2002). "Cognitive change and the APOE epsilon 4 allele". Nature 418 (6901): 932. doi:10.1038/418932a. PMID 12198535.
^ ^a ^b Farlow MR, He Y, Tekin S, Xu J, Lane R, Charles HC (2004). "Impact of APOE in mild cognitive impairment.". Neurology 63 (10): 1898–901. doi:10.1212/01.wnl.0000144279.21502.b7. PMID 15557508.
^ Burt TD, Agan BK, Marconi VC, He W, Kulkarni H, Mold JE, Cavrois M, Huang Y, Mahley RW, Dolan MJ, McCune JM, Ahuja SK (2008). "Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease progression". Proceedings of the National Academy of Sciences of the United States of America 105 (25): 8718–23. doi:10.1073/pnas.0803526105. PMID 18562290.
^ Chapman J, Vinokurov S, Achiron A, Karussis DM, Mitosek-Szewczyk K, Birnbaum M, Michaelson DM, Korczyn AD (2001). "APOE genotype is a major predictor of long-term progression of disability in MS". Neurology 56 (3): 312–6. doi:10.1212/wnl.56.3.312. PMID 11171894.
^ Schmidt S, Barcellos LF, DeSombre K, Rimmler JB, Lincoln RR, Bucher P, Saunders AM, Lai E, Martin ER, Vance JM, Oksenberg JR, Hauser SL, Pericak-Vance MA, Haines JL (2002). "Association of polymorphisms in the apolipoprotein E region with susceptibility to and progression of multiple sclerosis". American Journal of Human Genetics 70 (3): 708–17. doi:10.1086/339269. PMID 11836653.
^ Friedman G, Froom P, Sazbon L, Grinblatt I, Shochina M, Tsenter J, Babaey S, Yehuda B, Groswasser Z (1999). "Apolipoprotein E-epsilon4 genotype predicts a poor outcome in survivors of traumatic brain injury". Neurology 52 (2): 244–8. doi:10.1212/wnl.52.2.244. PMID 9932938.
^ McCarron MO, Delong D, Alberts MJ (1999). "APOE genotype as a risk factor for ischemic cerebrovascular disease: a meta-analysis". Neurology 53 (6): 1308–11. doi:10.1212/wnl.53.6.1308. PMID 10522889.
^ Kadotani H, Kadotani T, Young T, Peppard PE, Finn L, Colrain IM, Murphy GM, Mignot E (2001). "Association between apolipoprotein E epsilon4 and sleep-disordered breathing in adults". JAMA 285 (22): 2888–90. doi:10.1001/jama.285.22.2888. PMID 11401610.
^ Gottlieb DJ, DeStefano AL, Foley DJ, Mignot E, Redline S, Givelber RJ, Young T (2004). "APOE epsilon4 is associated with obstructive sleep apnea/hypopnea: the Sleep Heart Health Study.". Neurology 63 (4): 664–8. doi:10.1212/01.wnl.0000134671.99649.32. PMID 15326239.
^ Jacobs EG, Kroenke C, Lin J, Epel ES, Kenna HA, Blackburn EH, Rasgon NL (February 2013). "Accelerated cell aging in female APOE-ε4 carriers: implications for hormone therapy use.". PLOS ONE 8 (2): e54713. doi:10.1371/journal.pone.0054713. PMC 3572118. PMID 23418430.
^ Raber J (May 2008). "AR, apoE, and cognitive function". Horm Behav 53 (5): 706–15. doi:10.1016/j.yhbeh.2008.02.012. PMC 2409114. PMID 18395206.
^ Huebbe P, Nebel A, Siegert S, Moehring J, Boesch-Saadatmandi C, Most E, Pallauf J, Egert S, Müller MJ, Schreiber S, Nöthlings U, Rimbach G (September 2011). "APOE ε4 is associated with higher vitamin D levels in targeted replacement mice and humans.". FASEB J. 25 (9): 3262–70. doi:10.1096/fj.11-180935. PMID 21659554.
^ Sadigh-Eteghad S, Talebi M, Farhoudi M (2012). "Association of apolipoprotein E epsilon 4 allele with sporadic late onset Alzheimer’s disease, A meta-analysis". Neurosciences (Riyadh) 17 (4): 321–6. PMID 23022896.
^ Wisniewski T, Frangione B (1992). "Apolipoprotein E: A pathological chaperone protein in patients with cerebral and systemic amyloid". Neurosci. Lett. 135 (2): 235–238. doi:10.1016/0304-3940(92)90444-C. PMID 1625800.
^ Jiang Q, Lee CY, Mandrekar S, Wilkinson B, Cramer P, Zelcer N, Mann K, Lamb B, Willson TM, Collins JL, Richardson JC, Smith JD, Comery TA, Riddell D, Holtzman DM, Tontonoz P, Landreth GE (2008-06-12). "ApoE promotes the proteolytic degradation of Aβ". Neuron (United States: Cell Press) 58 (5): 681–93. doi:10.1016/j.neuron.2008.04.010. PMC 2493297. PMID 18549781. Lay summary – ScienceDaily (2008-06-13).
^ "Margaret Pericak-Vance, Ph.D.". Miami Institute of Human Genomics.
^ Pericak-Vance MA, Bebout JL, Gaskell PC, Yamaoka LH, Hung WY, Alberts MJ, Walker AP, Bartlett RJ, Haynes CA, Welsh KA (1991). "Linkage studies in familial Alzheimer disease: Evidence for chromosome 19 linkage". American Journal of Human Genetics 48 (6): 1034–50. PMC 1683100. PMID 2035524.
^ Hauser, Paul; Ryan, Robert (2013). "Impact of Apolipoprotein E on Alzheimer’s Disease". Current Alzheimer Research 10 (8): 809–817. doi:10.2174/15672050113109990156. ISSN 1567-2050. PMC 3995977.
^ Corder EH, Saunders AM, Risch NJ, Strittmatter WJ, Schmechel DE, Gaskell PC, Rimmler JB, Locke PA, Conneally PM, Schmader KE (1994). "Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease". Nat. Genet. 7 (2): 180–4. doi:10.1038/ng0694-180. PMID 7920638.
^ Farrer LA, Cupples LA, Haines JL, Hyman B, Kukull WA, Mayeux R, Myers RH, Pericak-Vance MA, Risch N, van Duijn CM (1997). JAMA 278: 1349–1356. doi:10.1001/jama.1997.03550160069041. PMID 9343467.

External links

Apolipoproteins E at the US National Library of Medicine Medical Subject Headings (MeSH)
apoe4.info - website for APOE-epsilon-4 carriers

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English Journal

Animal models to evaluate anti-atherosclerotic drugs.

Priyadharsini RP1.
Fundamental & clinical pharmacology.Fundam Clin Pharmacol.2015 Aug;29(4):329-40. doi: 10.1111/fcp.12130. Epub 2015 Jun 29.
Atherosclerosis is a multifactorial condition characterized by endothelial injury, fatty streak deposition, and stiffening of the blood vessels. The pathogenesis is complex and mediated by adhesion molecules, inflammatory cells, and smooth muscle cells. Statins have been the major drugs in treating
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Interleukin-18-induced atherosclerosis involves CD36 and NF-κB crosstalk in Apo E-/- mice.

Bhat OM1, Kumar PU2, Giridharan NV3, Kaul D1, Kumar MJ4, Dhawan V5.
Journal of cardiology.J Cardiol.2015 Jul;66(1):28-35. doi: 10.1016/j.jjcc.2014.10.012. Epub 2014 Dec 1.
OBJECTIVE: Interleukin (IL)-18 is a pleotropic cytokine involved in various inflammatory disorders. The transcription factor, nuclear factor kappa-B (NF-κB), is thought to play an important role in IL-18 signaling. The present study proposes a novel role for IL-18 in cholesterol efflux and plaque s
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Genetic Variation of ApoE Gene in Ethnic Kashmiri Population and Its Association with Outcome After Traumatic Brain Injury.

Yousuf A1, Khursheed N, Rasool I, Kundal V, Jeelani H, Afroze D.
Journal of molecular neuroscience : MN.J Mol Neurosci.2015 Jul;56(3):597-601. doi: 10.1007/s12031-015-0554-1. Epub 2015 Apr 10.
The outcome from traumatic brain injury (TBI) is variable and only partly explained by known prognostic factors. Genetic factors may influence the brain's susceptibility to injury or capacity for repair and regeneration. ApoE has been implicated in modifying neurological outcome after TBI, although
PMID 25859935

Japanese Journal

Enzyme assay for pyridoxal 5'-phosphate by apo-D-amino acid aminotransferase

Ota Hiroki,Mushiga Masuwo,Yoshimura Tohru [他]
Journal of bioscience and bioengineering 120(1), 117-119, 2015-07
NAID 40020538124

アポ化したD-アミノ酸アミノ基転移酵素を用いたピリドキサール5'-リン酸の測定法

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NAID 40020512652

FFI Reports 新規指定食品添加物β-アポ-8'-カロテナールの紹介

Foods & food ingredients journal of Japan : FFIジャーナル 220(2), 185-189, 2015
NAID 40020503679

Related Pictures

★リンクテーブル★

リンク元	「アポリポ蛋白E」「アポリポ蛋白質E」
関連記事	「apo」「Es」「E」

「アポリポ蛋白E」

Apolipoprotein E
	; PDB rendering based on 1b68.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1B68, 1BZ4, 1EA8, 1GS9, 1H7I, 1LE2, 1LE4, 1LPE, 1NFN, 1NFO, 1OEF, 1OEG, 1OR2, 1OR3, 2KC3, 2KNY, 2L7B
Identifiers
Symbols	APOE ; AD2; LDLCQ5; LPG
External IDs	OMIM: 107741 MGI: 88057 HomoloGene: 30951 GeneCards: APOE Gene
Gene ontology
Molecular function	• beta-amyloid binding; • lipid transporter activity; • protein binding; • phospholipid binding; • heparin binding; • lipid binding; • antioxidant activity; • cholesterol transporter activity; • identical protein binding; • protein homodimerization activity; • hydroxyapatite binding; • metal chelating activity; • tau protein binding; • low-density lipoprotein particle receptor binding; • phosphatidylcholine-sterol O-acyltransferase activator activity; • very-low-density lipoprotein particle receptor binding; • lipoprotein particle binding;
Cellular component	• extracellular region; • extracellular space; • nucleus; • cytoplasm; • early endosome; • late endosome; • Golgi apparatus; • plasma membrane; • membrane; • dendrite; • extrinsic component of external side of plasma membrane; • very-low-density lipoprotein particle; • low-density lipoprotein particle; • intermediate-density lipoprotein particle; • high-density lipoprotein particle; • chylomicron; • neuronal cell body; • extracellular vesicular exosome; • endocytic vesicle lumen; • blood microparticle;
Biological process	• response to reactive oxygen species; • retinoid metabolic process; • negative regulation of endothelial cell proliferation; • response to dietary excess; • triglyceride metabolic process; • cholesterol catabolic process; • cellular calcium ion homeostasis; • receptor-mediated endocytosis; • cytoskeleton organization; • G-protein coupled receptor signaling pathway; • nitric oxide mediated signal transduction; • synaptic transmission, cholinergic; • aging; • phototransduction, visible light; • cholesterol metabolic process; • cell death; • negative regulation of platelet activation; • positive regulation of cholesterol esterification; • positive regulation of cholesterol efflux; • peripheral nervous system axon regeneration; • long-chain fatty acid transport; • protein import; • cGMP-mediated signaling; • negative regulation of blood coagulation; • regulation of axon extension; • positive regulation of cGMP biosynthetic process; • regulation of Cdc42 protein signal transduction; • response to retinoic acid; • positive regulation of low-density lipoprotein particle receptor catabolic process; • response to insulin; • cholesterol efflux; • phospholipid efflux; • very-low-density lipoprotein particle remodeling; • low-density lipoprotein particle remodeling; • high-density lipoprotein particle remodeling; • high-density lipoprotein particle assembly; • chylomicron remnant clearance; • high-density lipoprotein particle clearance; • very-low-density lipoprotein particle clearance; • lipoprotein metabolic process; • lipoprotein biosynthetic process; • lipoprotein catabolic process; • vasodilation; • cholesterol homeostasis; • negative regulation of MAP kinase activity; • negative regulation of neuron apoptotic process; • negative regulation of blood vessel endothelial cell migration; • reverse cholesterol transport; • small molecule metabolic process; • response to ethanol; • negative regulation of cholesterol biosynthetic process; • positive regulation of axon extension; • positive regulation of lipid biosynthetic process; • intracellular transport; • regulation of neuronal synaptic plasticity; • oligodendrocyte differentiation; • artery morphogenesis; • negative regulation of inflammatory response; • positive regulation of nitric-oxide synthase activity; • positive regulation of membrane protein ectodomain proteolysis; • negative regulation of lipid biosynthetic process; • maintenance of location in cell; • fatty acid homeostasis; • positive regulation of dendritic spine development; • negative regulation of dendritic spine development; • cellular response to interleukin-1; • cellular response to growth factor stimulus; • cellular response to cholesterol; • negative regulation of cholesterol efflux; • alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate selective glutamate receptor clustering; • N-methyl-D-aspartate receptor clustering; • regulation of beta-amyloid clearance; • regulation of neuron death; • negative regulation of neuron death; • positive regulation of neuron death; • negative regulation of postsynaptic membrane organization; • positive regulation of postsynaptic membrane organization; • negative regulation of presynaptic membrane organization; • positive regulation of presynaptic membrane organization; • positive regulation of beta-amyloid formation; • negative regulation of beta-amyloid formation; • regulation of tau-protein kinase activity; • negative regulation of dendritic spine maintenance; • positive regulation of dendritic spine maintenance; • positive regulation of phospholipid efflux; • positive regulation of neurofibrillary tangle assembly; • negative regulation of phospholipid efflux; • negative regulation of lipid transport across blood brain barrier; • positive regulation of lipid transport across blood brain barrier;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
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