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MHC class I

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397:). Calnexin acts to stabilize the class I MHC α chains prior to β2m binding. Following complete assembly of the MHC molecule, calnexin dissociates. The MHC molecule lacking a bound peptide is inherently unstable and requires the binding of the chaperones calreticulin and Erp57. Additionally, tapasin binds to the MHC molecule and serves to link it to the TAP proteins and facilitates the selection of peptide in an iterative process called peptide editing, thus facilitating enhanced peptide loading and colocalization. 466:(NK) cells are normally inactivated upon recognizing MHC I molecules on the surface of cells. Therefore, in the absence of MHC I molecules, NK cells are activated and recognize the cell as aberrant, suggesting that it may be infected by viruses attempting to evade immune destruction. Several human cancers also show down-regulation of MHC I, giving transformed cells the same survival advantage of being able to avoid normal immune surveillance designed to destroy any infected or transformed cells. 311: 31: 451:. As viruses induce cellular expression of viral proteins, some of these products are tagged for degradation, with the resulting peptide fragments entering the endoplasmic reticulum and binding to MHC I molecules. It is in this way, the MHC class I-dependent pathway of antigen presentation, that the virus infected cells signal T-cells that abnormal proteins are being produced as a result of infection. 330:
activity. The proteasome degrades intracellular proteins into small peptides that are then released into the cytosol. Proteasomes can also ligate distinct peptide fragments (termed spliced peptides), producing sequences that are noncontiguous and therefore not linearly templated in the genome. The
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A normal cell will display peptides from normal cellular protein turnover on its class I MHC, and CTLs will not be activated in response to them due to central and peripheral tolerance mechanisms. When a cell expresses foreign proteins, such as after viral infection, a fraction of the class I MHC
627:(death) of one copy of the gene, though sometimes this process results in two new genes with divergent function. It is likely that human MHC class Ib loci (HLA-E, -F, and -G) as well as MHC class I pseudogenes arose from MHC class Ia loci (HLA-A, -B, and -C) in this birth-and-death process. 462:, reducing the risk of infecting neighboring cells. As an evolutionary response to this method of immune surveillance, many viruses are able to down-regulate or otherwise prevent the presentation of MHC class I molecules on the cell surface. In contrast to cytotoxic T lymphocytes, 153:. The MHC I: peptide complex is then inserted via the endoplasmic reticulum into the external plasma membrane of the cell. The epitope peptide is bound on extracellular parts of the class I MHC molecule. Thus, the function of the class I MHC is to display intracellular proteins to 286:
domains fold to make up a groove for peptides to bind. MHC class I molecules bind peptides that are predominantly 8-10 amino acid in length (Parham 87), but the binding of longer peptides have also been reported.
587:, and have been found in all living jawed vertebrates that have been studied thus far. Since their emergence in jawed vertebrates, this gene family has been subjected to many divergent evolutionary paths as 1407:
Albring J, Koopmann JO, Hämmerling GJ, Momburg F (January 2004). "Retrotranslocation of MHC class I heavy chain from the endoplasmic reticulum to the cytosol is dependent on ATP supply to the ER lumen".
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Kulski JK, Shiina T, Anzai T, Kohara S, Inoko H (December 2002). "Comparative genomic analysis of the MHC: the evolution of class I duplication blocks, diversity and complexity from shark to man".
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Simplified diagram of cytoplasmic protein degradation by the proteasome, transport into endoplasmic reticulum by TAP complex, loading on MHC class I, and transport to the surface for presentation
102:; this will trigger an immediate response from the immune system against a particular non-self antigen displayed with the help of an MHC class I protein. Because MHC class I molecules present 1710: 331:
origin of spliced peptide segments can be from the same protein (cis-splicing) or different proteins (trans-splicing). The peptides have to be translocated from the cytosol into the
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Wearsch PA, Cresswell P (August 2007). "Selective loading of high-affinity peptides onto major histocompatibility complex class I molecules by the tapasin-ERp57 heterodimer".
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Faridi P, Li C, Ramarathinam SH, Vivian JP, Illing PT, Mifsud NA, Ayala R, Song J, Gearing LJ, Hertzog PJ, Ternette N, Rossjohn J, Croft NP, Purcell AW (12 October 2018).
172:(NKs). Reduction in the normal levels of surface class I MHC, a mechanism employed by some viruses and certain tumors to evade CTL responses, activates NK cell killing. 366:. The two subunits form a peptide binding site and two ATP binding sites that face the cytosol. TAP binds peptides on the cytoplasmic side and translocates them under 1703: 428:
channel into the cytosol, where they might undergo further trimming in size, and might be translocated by TAP back into ER for binding to a MHC class I molecule.
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Blees A, Januliene D, Hofmann T, Koller N, Schmidt C, Trowitzsch S, Moeller A, Tampé R (November 2017). "Structure of the human MHC-I peptide-loading complex".
1696: 1486:"Activation of CXCR4 triggers ubiquitination and down-regulation of major histocompatibility complex class I (MHC-I) on epithelioid carcinoma HeLa cells" 623:
events cause the genome to contain multiple copies of a gene which can then undergo separate evolutionary processes. Sometimes these processes result in
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will display these peptides on the cell surface. Consequently, CTLs specific for the MHC:peptide complex will recognize and kill presenting cells.
1527:"Trans-species polymorphism in humans and the great apes is generally maintained by balancing selection that modulates the host immune response" 1053: 351: 2091: 2096: 1445:"Exogenous antigens are processed through the endoplasmic reticulum-associated degradation (ERAD) in cross-presentation by dendritic cells" 2594: 1368:"Export of antigenic peptides from the endoplasmic reticulum intersects with retrograde protein translocation through the Sec61p channel" 893:
Ljunggren HG, Stam NJ, Öhlén C, Neefjes JJ, Höglund P, Heemels MT, Bastin J, Schumacher TN, Townsend A, Kärre K, Ploegh HL (1990-08-02).
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Peptides that fail to bind MHC class I molecules in the lumen of the endoplasmic reticulum (ER) are removed from the ER via the
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Sun Y, Young MC, Woodward CH, Danon JN, Truong HV, Gupta S, Winters TJ, Font-Burgada J, Burslem GM, Sgourakis NG (2023-06-20).
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consumption into the lumen of the ER. The MHC class I molecule is then, in turn, loaded with peptides in the lumen of the ER.
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Syken J, Grandpre T, Kanold PO, Shatz CJ (September 2006). "PirB restricts ocular-dominance plasticity in visual cortex".
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Liepe J, Marino F, Sidney J, Jeko A, Bunting DE, Sette A, Kloetzel PM, Stumpf MP, Heck AJ, Mishto M (21 October 2016).
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to reach the cell surface. The transport of the MHC class I molecules through the secretory pathway involves several
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Once the peptide is loaded onto the MHC class I molecule, the complex dissociates and it leaves the ER through the
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Koopmann JO, Albring J, Hüter E, Bulbuc N, Spee P, Neefjes J, Hämmerling GJ, Momburg F, et al. (July 2000).
1319:"Tapasin shapes immunodominance hierarchies according to the kinetic stability of peptide-MHC class I complexes" 858:
Burrows SR, Rossjohn J, McCluskey J (January 2006). "Have we cut ourselves too short in mapping CTL epitopes?".
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Paired-immunoglobulin-like receptor B (PirB), an MHCI-binding receptor, is involved in the regulation of visual
157:(CTLs). However, class I MHC can also present peptides generated from exogenous proteins, in a process known as 1668: 1097: 1054:"A subset of HLA-I peptides are not genomically templated: Evidence for cis- and trans-spliced peptide ligands" 405: 989:"Universal open MHC-I molecules for rapid peptide loading and enhanced complex stability across HLA allotypes" 757:
Hansen TH, Bouvier M (July 2009). "MHC class I antigen presentation: learning from viral evasion strategies".
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between the peptide, MHC I, and B2M, under subphysiological temperatures, stable, peptide-deficient MHC I/B2M
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The peptide-loading process involves several other molecules that form a large multimeric complex called the
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in an evolutionary related MHC class I gene remains in two species, likely due to strong pathogen-mediated
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of the MHC molecule. Some of the posttranslational modifications occur in the ER and involve change to the
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http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/H/HLA.html#Class_I_Histocompatibility_Molecules
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have been observed. Synthetic stable, peptide-receptive MHC I molecules have been generated using a
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Thirdborough SM, Roddick JS, Radcliffe JN, Howarth M, Stevenson FK, Elliott T (February 2008).
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evolution is one of the mechanistic explanations for the size of the MHC class I gene family.
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became more pronounced at all ages. PirB loss of function mutant mice also exhibited enhanced
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While a high-affinity peptide and the B2M subunit are normally required to maintain a stable
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The peptide translocation from the cytosol into the lumen of the ER is accomplished by the
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MHC class I molecules are heterodimers that consist of two polypeptide chains, α and
99: 98:. Their function is to display peptide fragments of proteins from within the cell to 1352: 1303: 1150: 724: 2076: 1638: 1597: 1589: 1548: 1538: 1497: 1456: 1417: 1379: 1330: 1283: 1246: 1236: 1201: 1181: 1128: 1120: 1098:"A large fraction of HLA class I ligands are proteasome-generated spliced peptides" 1068: 1024: 1008: 961: 948:
Schumacher TN, Heemels MT, Neefjes JJ, Kast W, Melief CJ, Ploegh HL (August 1990).
914: 867: 844: 824: 786: 766: 704: 664: 656: 645:"The MHC class I antigen presentation pathway: strategies for viral immune evasion" 620: 200: 189: 154: 1217:"Tapasin enhances MHC class I peptide presentation according to peptide half-life" 2490: 2009: 1872: 1726: 1421: 744: 443:
MHC class I molecules are loaded with peptides generated from the degradation of
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Proceedings of the National Academy of Sciences of the United States of America
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events have taken place. There are, however, documented cases of trans-species
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family and is a heterodimeric multimembrane-spanning polypeptide consisting of
299: 238:(B2M). The two chains are linked noncovalently via interaction of B2M and the α 95: 1543: 412:
regions of the protein, followed by extensive changes to the N-glycans in the
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heterodimer ligand, and checks the coupled peptide for antigenicity. The α
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and adulthood. When the function of PirB was abolished in mutant mice,
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Alternatively, class I MHC itself can serve as an inhibitory ligand for
624: 588: 323: 214:. These results suggest that PirB may be involved in the modulation of 150: 87: 2050: 918: 455: 83: 1484:
Wang Z, Zhang L, Qiao A, Watson K, Zhang J, Fan GH (February 2008).
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generated mainly from the degradation of cytosolic proteins by the
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The fate of the virus-infected cell is almost always induction of
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proteins, the pathway of MHC class I presentation is often called
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Imai J, Hasegawa H, Maruya M, Koyasu S, Yahara I (January 2005).
432: 416:. The N-glycans mature fully before they reach the cell surface. 378: 319: 146: 107: 103: 1406: 2475: 2443: 2426: 2409: 2392: 2290: 2285: 2280: 2275: 2270: 2260: 2255: 2250: 2245: 2240: 1973: 1964: 1857: 1578:"Concerted and birth-and-death evolution of multigene families" 596: 259: 1214: 246:, while the B2M subunit is not polymorphic and encoded by the 30: 2374: 2369: 2364: 2359: 2354: 2349: 1945: 1941: 1215:
Howarth M, Williams A, Tolstrup AB, Elliott T (August 2004).
549: 537: 525: 508: 496: 484: 425: 394: 390: 266:-CD8 interaction holds the MHC I molecule in place while the 134: 130: 126: 2331: 1525:
Azevedo L, Serrano C, Amorim A, Cooper DN (September 2015).
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domain is plasma membrane-spanning and interacts with the
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domain. Only the α chain is polymorphic and encoded by a
1442: 857: 806: 270:(TCR) on the surface of the cytotoxic T cell binds its α 694: 614: 1095: 986: 747:
Kimball's Biology Pages, Histocompatibility Molecules
345: 1483: 895:"Empty MHC class I molecules come out in the cold" 1627:"Origin and evolution of HLA class I pseudogenes" 431:For example, an interaction of sec61 with bovine 2566: 1273: 993:Proceedings of the National Academy of Sciences 302:between the MHC I and B2M, named "open MHC-I". 352:transporter associated with antigen processing 2317: 1704: 756: 579:The MHC class I genes originated in the most 175: 1436: 1400: 1359: 802: 800: 798: 796: 2324: 2310: 1711: 1697: 29: 1681:at the U.S. National Library of Medicine 1671:at the U.S. National Library of Medicine 1642: 1601: 1575: 1552: 1542: 1501: 1460: 1383: 1334: 1250: 1240: 1132: 1072: 1028: 793: 668: 595:in MHC class I genes, where a particular 318:The peptides are generated mainly in the 309: 619:Birth-and-death evolution asserts that 574: 339:of the ER. They have membrane proximal 210:after monocular deprivation during the 35:Schematic representation of MHC class I 2567: 1624: 1594:10.1146/annurev.genet.39.073003.112240 642: 2305: 1692: 1644:10.1093/oxfordjournals.molbev.a040201 469: 690: 688: 615:Birth-and-death of MHC class I genes 438: 1669:Histocompatibility+Antigens+Class+I 1490:The Journal of Biological Chemistry 13: 2595:Single-pass transmembrane proteins 419: 70:are one of two primary classes of 14: 2606: 1837:Polymeric immunoglobulin receptor 1662: 685: 346:Translocation and peptide loading 125:corresponding to MHC class I are 74:(MHC) molecules (the other being 2524:Minor histocompatibility antigen 2333:Major histocompatibility complex 709:10.1034/j.1600-065x.2002.19008.x 661:10.1046/j.1365-2567.2003.01738.x 72:major histocompatibility complex 1631:Molecular Biology and Evolution 1618: 1576:Nei M, Rooney AP (2005-11-14). 1569: 1518: 1477: 1310: 1267: 1208: 1157: 1089: 1045: 406:posttranslational modifications 2049:(with two glycoprotein chains 1323:European Journal of Immunology 980: 941: 886: 851: 750: 731: 636: 607:that can infect both species. 354:(TAP). TAP is a member of the 1: 2145:Killer-cell IG-like receptors 1385:10.1016/S1074-7613(00)00013-3 630: 1422:10.1016/j.molimm.2003.08.008 966:10.1016/0092-8674(90)90020-F 305: 225: 16:Protein of the immune system 7: 2233:Leukocyte IG-like receptors 184:. PirB is expressed in the 145:Class I MHC molecules bind 140: 10: 2611: 2554:Cluster of differentiation 1724:immunoglobulin superfamily 1074:10.1126/sciimmunol.aar3947 759:Nature Reviews. Immunology 643:Hewitt EW (October 2003). 176:PirB and visual plasticity 2544:Human blood group systems 2511: 2383: 2340: 2231: 2143: 2122: 2069: 2037: 2002: 1972: 1963: 1934: 1914: 1890: 1881: 1865: 1856: 1849: 1829: 1806: 1773: 1744: 1733: 1582:Annual Review of Genetics 1544:10.1186/s40246-015-0043-1 53: 45: 40: 28: 23: 1683:Medical Subject Headings 1673:Medical Subject Headings 1625:Hughes AL (March 1995). 1449:International Immunology 872:10.1016/j.it.2005.11.001 2549:Cell adhesion molecules 2519:Human leukocyte antigen 1720:Transmembrane receptors 1242:10.1073/pnas.0306294101 1125:10.1126/science.aaf4384 1013:10.1073/pnas.2304055120 829:10.1126/science.1128232 375:Peptide loading complex 86:cells in the bodies of 78:) and are found on the 1503:10.1074/jbc.m706848200 581:recent common ancestor 460:cell-mediated immunity 447:cytosolic proteins in 315: 186:central nervous system 1462:10.1093/intimm/dxh184 1336:10.1002/eji.200737832 697:Immunological Reviews 333:endoplasmic reticulum 313: 195:in the developmental 90:. They also occur on 68:MHC class I molecules 1410:Molecular Immunology 860:Trends in Immunology 575:Evolutionary history 248:Beta-2 microglobulin 170:natural killer cells 2070:Accessory molecules 1935:Accessory molecules 1233:2004PNAS..10111737H 1186:10.1038/nature24627 1178:2017Natur.551..525B 1117:2016Sci...354..354L 1005:2023PNAS..12004055S 999:(25): e2304055120. 911:1990Natur.346..476L 821:2006Sci...313.1795S 601:balancing selection 435:has been observed. 377:consisting of TAP, 216:synaptic plasticity 2134:cytokine receptors 1734:Antibody receptor: 1061:Science Immunology 815:(5794): 1795–800. 743:2016-02-04 at the 470:Genes and isotypes 316: 159:cross-presentation 116:endogenous pathway 2590:Protein targeting 2562: 2561: 2529:Blood transfusion 2299: 2298: 2124:Cytokine receptor 2118: 2117: 2114: 2113: 1959: 1958: 1930: 1929: 1845: 1844: 1679:MHC+Class+I+Genes 1276:Nature Immunology 1172:(7681): 525–528. 1111:(6310): 354–358. 905:(6283): 476–480. 585:jawed vertebrates 516:Less polymorphic 475:Very polymorphic 439:Effect of viruses 402:secretory pathway 155:cytotoxic T cells 100:cytotoxic T cells 65: 64: 2602: 2326: 2319: 2312: 2303: 2302: 2003:Antigen receptor 1970: 1969: 1888: 1887: 1866:Antigen receptor 1863: 1862: 1854: 1853: 1850:Antigen receptor 1808:Alpha (α)/mu (μ) 1742: 1741: 1727:immune receptors 1713: 1706: 1699: 1690: 1689: 1657: 1656: 1646: 1622: 1616: 1615: 1605: 1573: 1567: 1566: 1556: 1546: 1522: 1516: 1515: 1505: 1481: 1475: 1474: 1464: 1440: 1434: 1433: 1404: 1398: 1397: 1387: 1363: 1357: 1356: 1338: 1314: 1308: 1307: 1271: 1265: 1264: 1254: 1244: 1227:(32): 11737–42. 1212: 1206: 1205: 1161: 1155: 1154: 1136: 1102: 1093: 1087: 1086: 1076: 1067:(28): eaar3947. 1058: 1049: 1043: 1042: 1032: 984: 978: 977: 945: 939: 938: 919:10.1038/346476a0 890: 884: 883: 855: 849: 848: 804: 791: 790: 754: 748: 735: 729: 728: 692: 683: 682: 672: 640: 625:pseudogenization 621:gene duplication 201:ocular dominance 190:ocular dominance 33: 21: 20: 2610: 2609: 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2520: 2517: 2516: 2514: 2510: 2502: 2499: 2497: 2494: 2492: 2489: 2487: 2484: 2482: 2479: 2478: 2477: 2474: 2470: 2467: 2465: 2462: 2460: 2457: 2455: 2452: 2450: 2447: 2446: 2445: 2442: 2438: 2435: 2433: 2430: 2429: 2428: 2425: 2421: 2418: 2416: 2413: 2412: 2411: 2408: 2404: 2401: 2399: 2396: 2395: 2394: 2391: 2390: 2388: 2386: 2382: 2376: 2373: 2371: 2368: 2366: 2363: 2361: 2358: 2356: 2353: 2351: 2348: 2347: 2345: 2343: 2339: 2334: 2327: 2322: 2320: 2315: 2313: 2308: 2307: 2304: 2292: 2289: 2287: 2284: 2282: 2279: 2277: 2274: 2272: 2269: 2267: 2264: 2262: 2259: 2257: 2254: 2252: 2249: 2247: 2244: 2242: 2239: 2238: 2236: 2234: 2230: 2224: 2221: 2219: 2216: 2214: 2211: 2209: 2206: 2204: 2201: 2199: 2196: 2194: 2191: 2189: 2186: 2184: 2181: 2179: 2176: 2174: 2171: 2169: 2166: 2164: 2161: 2159: 2156: 2154: 2151: 2150: 2148: 2146: 2142: 2136: 2135: 2130: 2129: 2127: 2125: 2121: 2106: 2102: 2099:(also called 2098: 2095: 2093: 2090: 2088: 2085: 2083: 2080: 2078: 2075: 2074: 2072: 2068: 2062: 2059: 2056: 2052: 2048: 2045: 2044: 2042: 2040: 2036: 2030: 2027: 2025: 2022: 2020: 2017: 2015: 2011: 2008: 2007: 2005: 2001: 1993: 1990: 1988: 1985: 1984: 1983: 1980: 1979: 1977: 1975: 1971: 1968: 1966: 1962: 1951: 1947: 1943: 1940: 1939: 1937: 1933: 1923: 1920: 1919: 1917: 1913: 1907: 1903: 1899: 1896: 1895: 1893: 1889: 1886: 1884: 1880: 1874: 1871: 1870: 1868: 1864: 1861: 1859: 1855: 1852: 1848: 1838: 1835: 1834: 1832: 1828: 1822: 1819: 1817: 1814: 1813: 1811: 1809: 1805: 1799: 1796: 1794: 1791: 1789: 1786: 1784: 1781: 1780: 1778: 1776: 1772: 1765: 1764:C-type lectin 1761: 1757: 1755: 1752: 1751: 1749: 1747: 1743: 1740: 1738: 1732: 1728: 1725: 1721: 1714: 1709: 1707: 1702: 1700: 1695: 1694: 1691: 1684: 1680: 1677: 1674: 1670: 1667: 1666: 1654: 1650: 1645: 1640: 1637:(2): 247–58. 1636: 1632: 1628: 1621: 1613: 1609: 1604: 1599: 1595: 1591: 1588:(1): 121–52. 1587: 1583: 1579: 1572: 1564: 1560: 1555: 1550: 1545: 1540: 1536: 1532: 1528: 1521: 1513: 1509: 1504: 1499: 1496:(7): 3951–9. 1495: 1491: 1487: 1480: 1472: 1468: 1463: 1458: 1454: 1450: 1446: 1439: 1431: 1427: 1423: 1419: 1415: 1411: 1403: 1395: 1391: 1386: 1381: 1378:(1): 117–27. 1377: 1373: 1369: 1362: 1354: 1350: 1346: 1342: 1337: 1332: 1328: 1324: 1320: 1313: 1305: 1301: 1297: 1293: 1289: 1285: 1282:(8): 873–81. 1281: 1277: 1270: 1262: 1258: 1253: 1248: 1243: 1238: 1234: 1230: 1226: 1222: 1218: 1211: 1203: 1199: 1195: 1191: 1187: 1183: 1179: 1175: 1171: 1167: 1160: 1152: 1148: 1144: 1140: 1135: 1134:10044/1/42330 1130: 1126: 1122: 1118: 1114: 1110: 1106: 1099: 1092: 1084: 1080: 1075: 1070: 1066: 1062: 1055: 1048: 1040: 1036: 1031: 1026: 1022: 1018: 1014: 1010: 1006: 1002: 998: 994: 990: 983: 975: 971: 967: 963: 959: 955: 951: 944: 936: 932: 928: 924: 920: 916: 912: 908: 904: 900: 896: 889: 881: 877: 873: 869: 865: 861: 854: 846: 842: 838: 834: 830: 826: 822: 818: 814: 810: 803: 801: 799: 797: 788: 784: 780: 776: 772: 768: 765:(7): 503–13. 764: 760: 753: 746: 742: 739: 734: 726: 722: 718: 714: 710: 706: 702: 698: 691: 689: 680: 676: 671: 666: 662: 658: 654: 650: 646: 639: 635: 628: 626: 622: 612: 610: 606: 602: 598: 594: 593:polymorphisms 590: 586: 582: 567: 566: 562: 559: 558: 554: 551: 547: 546: 542: 539: 535: 534: 530: 527: 523: 522: 518: 517: 515: 510: 506: 505: 501: 498: 494: 493: 489: 486: 482: 481: 477: 476: 474: 473: 467: 465: 461: 457: 452: 450: 446: 445:ubiquitinated 436: 434: 429: 427: 417: 415: 411: 407: 403: 398: 396: 392: 388: 384: 380: 376: 371: 369: 365: 361: 357: 353: 343: 342: 338: 334: 329: 325: 321: 312: 303: 301: 297: 293: 288: 269: 261: 257: 249: 245: 237: 223: 221: 220:visual cortex 217: 213: 209: 205: 202: 198: 194: 191: 187: 183: 173: 171: 166: 162: 160: 156: 152: 148: 138: 136: 132: 128: 124: 119: 117: 113: 109: 106:derived from 105: 101: 97: 94:, but not on 93: 89: 85: 81: 77: 73: 69: 61: 58: 56: 52: 48: 44: 39: 32: 27: 22: 19: 2385:MHC class II 2341: 2131: 2039:Co-receptors 1992:MHC class II 1986: 1634: 1630: 1620: 1585: 1581: 1571: 1534: 1530: 1520: 1493: 1489: 1479: 1455:(1): 45–53. 1452: 1448: 1438: 1413: 1409: 1402: 1375: 1371: 1361: 1329:(2): 364–9. 1326: 1322: 1312: 1279: 1275: 1269: 1224: 1220: 1210: 1169: 1165: 1159: 1108: 1104: 1091: 1064: 1060: 1047: 996: 992: 982: 957: 953: 943: 902: 898: 888: 863: 859: 853: 812: 808: 762: 758: 752: 733: 700: 696: 655:(2): 163–9. 652: 648: 638: 618: 578: 568:(pseudogene) 563: 560:(pseudogene) 555: 543: 531: 519: 502: 490: 478: 453: 442: 430: 423: 399: 383:calreticulin 372: 349: 317: 296:heterodimers 289: 229: 179: 167: 163: 144: 120: 115: 111: 80:cell surface 76:MHC class II 67: 66: 18: 2539:Calgranulin 2342:MHC class I 1987:MHC class I 1883:Co-receptor 1746:Epsilon (ε) 1737:Fc receptor 866:(1): 11–6. 449:proteasomes 328:proteolytic 250:gene. The α 88:vertebrates 49:MHC class I 41:Identifiers 24:MHC class I 2569:Categories 1891:stimulate: 703:: 95–122. 649:Immunology 631:References 589:speciation 324:proteasome 208:plasticity 204:plasticity 193:plasticity 182:plasticity 151:proteasome 55:Membranome 1830:Secretory 1775:Gamma (γ) 1537:(1): 21. 1021:0027-8424 927:0028-0836 605:pathogens 456:apoptosis 306:Synthesis 226:Structure 112:cytosolic 108:cytosolic 92:platelets 84:nucleated 2534:Arrestin 2178:KIR2DL5B 2173:KIR2DL5A 1915:inhibit: 1798:Neonatal 1612:16285855 1563:26337052 1512:18083706 1471:15546887 1430:14644099 1394:10933400 1372:Immunity 1353:28659293 1345:18196518 1304:29762957 1296:17603487 1261:15286279 1194:29107940 1151:41095551 1143:27846572 1083:30315122 1039:37310998 1030:10288639 880:16297661 837:16917027 779:19498380 741:Archived 725:41765680 717:12493009 679:14511229 458:through 410:N-glycan 387:calnexin 244:HLA gene 147:peptides 141:Function 104:peptides 2335:classes 2223:KIR3DS1 2218:KIR3DL3 2213:KIR3DL2 2208:KIR3DL1 2203:KIR2DS5 2198:KIR2DS4 2193:KIR2DS3 2188:KIR2DS2 2183:KIR2DS1 2168:KIR2DL4 2163:KIR2DL3 2158:KIR2DL2 2153:KIR2DL1 2097:ζ-chain 1974:Ligands 1965:T cells 1858:B cells 1793:FcγRIII 1653:7700152 1603:1464479 1554:4559023 1229:Bibcode 1202:4447406 1174:Bibcode 1113:Bibcode 1105:Science 1001:Bibcode 974:2199065 935:2198471 907:Bibcode 845:1860730 817:Bibcode 809:Science 787:9278263 670:1783040 583:of all 433:albumin 379:tapasin 341:Ig fold 322:by the 320:cytosol 262:. The α 260:T-cells 218:in the 82:of all 2476:HLA-DR 2444:HLA-DQ 2427:HLA-DP 2410:HLA-DO 2393:HLA-DM 2291:LILRB5 2286:LILRB4 2281:LILRB3 2276:LILRB2 2271:LILRB1 2266:LILRA6 2261:LILRA5 2256:LILRA4 2251:LILRA3 2246:LILRA2 2241:LILRA1 1821:Fcα/μR 1788:FcγRII 1760:FcεRII 1685:(MeSH) 1675:(MeSH) 1651:  1610:  1600:  1561:  1551:  1510:  1469:  1428:  1392:  1351:  1343:  1302:  1294:  1259:  1252:511045 1249:  1200:  1192:  1166:Nature 1149:  1141:  1081:  1037:  1027:  1019:  972:  933:  925:  899:Nature 878:  843:  835:  785:  777:  723:  715:  677:  667:  597:allele 389:, and 133:, and 46:Symbol 2575:Genes 2512:Other 2375:HLA-G 2370:HLA-F 2365:HLA-E 2360:HLA-C 2355:HLA-B 2350:HLA-A 1816:FcαRI 1783:FcγRI 1754:FcεRI 1349:S2CID 1300:S2CID 1198:S2CID 1147:S2CID 1101:(PDF) 1057:(PDF) 841:S2CID 783:S2CID 721:S2CID 565:HLA-L 557:HLA-K 550:HLA-G 545:HLA-G 538:HLA-F 533:HLA-F 526:HLA-E 521:HLA-E 509:HLA-C 504:HLA-C 497:HLA-B 492:HLA-B 485:HLA-A 480:HLA-A 426:sec61 395:PDIA3 391:Erp57 337:lumen 282:and α 135:HLA-C 131:HLA-B 127:HLA-A 2132:see 2105:TCRζ 2103:and 2101:CD3ζ 2092:CD3ε 2087:CD3δ 2082:CD3γ 2055:CD8β 2053:and 2051:CD8α 2029:TRG@ 2024:TRD@ 2019:TRB@ 2014:TRA@ 1950:CD79 1946:Ig-β 1942:Ig-α 1922:CD22 1906:CD81 1902:CD19 1898:CD21 1649:PMID 1608:PMID 1559:PMID 1508:PMID 1467:PMID 1426:PMID 1390:PMID 1341:PMID 1292:PMID 1257:PMID 1190:PMID 1139:PMID 1079:PMID 1035:PMID 1017:ISSN 970:PMID 954:Cell 931:PMID 923:ISSN 876:PMID 833:PMID 775:PMID 713:PMID 675:PMID 364:TAP2 362:and 360:TAP1 123:HLAs 2077:CD3 2061:CD4 2047:CD8 2010:TCR 1982:MHC 1873:BCR 1762:is 1639:doi 1598:PMC 1590:doi 1549:PMC 1539:doi 1498:doi 1494:283 1457:doi 1418:doi 1380:doi 1331:doi 1284:doi 1247:PMC 1237:doi 1225:101 1182:doi 1170:551 1129:hdl 1121:doi 1109:354 1069:doi 1025:PMC 1009:doi 997:120 962:doi 915:doi 903:346 868:doi 825:doi 813:313 767:doi 705:doi 701:190 665:PMC 657:doi 653:110 603:by 368:ATP 256:CD8 114:or 2571:: 2501:β5 2496:β4 2491:β3 2486:β1 2469:β3 2464:β2 2459:β1 2454:α2 2449:α1 2437:β1 2432:α1 2012:: 1722:: 1647:. 1635:12 1633:. 1629:. 1606:. 1596:. 1586:39 1584:. 1580:. 1557:. 1547:. 1533:. 1529:. 1506:. 1492:. 1488:. 1465:. 1453:17 1451:. 1447:. 1424:. 1414:40 1412:. 1388:. 1376:13 1374:. 1370:. 1347:. 1339:. 1327:38 1325:. 1321:. 1298:. 1290:. 1278:. 1255:. 1245:. 1235:. 1223:. 1219:. 1196:. 1188:. 1180:. 1168:. 1145:. 1137:. 1127:. 1119:. 1107:. 1103:. 1077:. 1063:. 1059:. 1033:. 1023:. 1015:. 1007:. 995:. 991:. 968:. 958:62 956:. 952:. 929:. 921:. 913:. 901:. 897:. 874:. 864:27 862:. 839:. 831:. 823:. 811:. 795:^ 781:. 773:. 761:. 719:. 711:. 699:. 687:^ 673:. 663:. 651:. 647:. 385:, 381:, 274:-α 222:. 161:. 137:. 129:, 118:. 60:63 2481:α 2420:β 2415:α 2403:β 2398:α 2325:e 2318:t 2311:v 2107:) 2057:) 1952:) 1948:( 1944:/ 1904:/ 1900:/ 1766:) 1758:( 1712:e 1705:t 1698:v 1655:. 1641:: 1614:. 1592:: 1565:. 1541:: 1535:9 1514:. 1500:: 1473:. 1459:: 1432:. 1420:: 1396:. 1382:: 1355:. 1333:: 1306:. 1286:: 1280:8 1263:. 1239:: 1231:: 1204:. 1184:: 1176:: 1153:. 1131:: 1123:: 1115:: 1085:. 1071:: 1065:3 1041:. 1011:: 1003:: 976:. 964:: 937:. 917:: 909:: 882:. 870:: 847:. 827:: 819:: 789:. 769:: 763:9 727:. 707:: 681:. 659:: 552:) 548:( 540:) 536:( 528:) 524:( 511:) 507:( 499:) 495:( 487:) 483:( 393:( 284:2 280:1 276:2 272:1 264:3 252:3 240:3 234:2 232:β

Index


Membranome
63
major histocompatibility complex
MHC class II
cell surface
nucleated
vertebrates
platelets
red blood cells
cytotoxic T cells
peptides
cytosolic
HLAs
HLA-A
HLA-B
HLA-C
peptides
proteasome
cytotoxic T cells
cross-presentation
natural killer cells
plasticity
central nervous system
ocular dominance
plasticity
critical period
ocular dominance
plasticity
plasticity

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