2xpg

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{{STRUCTURE_2xpg| PDB=2xpg | SCENE= }}
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==Crystal structure of a MHC class I-peptide complex==
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===Crystal structure of a MHC class I-peptide complex===
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<StructureSection load='2xpg' size='340' side='right' caption='[[2xpg]], [[Resolution|resolution]] 2.60&Aring;' scene=''>
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{{ABSTRACT_PUBMED_21543847}}
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== Structural highlights ==
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<table><tr><td colspan='2'>[[2xpg]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2XPG OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2XPG FirstGlance]. <br>
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</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1uqs|1uqs]], [[1bd2|1bd2]], [[2esv|2esv]], [[2xks|2xks]], [[2ak4|2ak4]], [[1ypz|1ypz]], [[1im3|1im3]], [[1uxw|1uxw]], [[1i7u|1i7u]], [[1c16|1c16]], [[1hsa|1hsa]], [[2axf|2axf]], [[1gzp|1gzp]], [[2bnq|2bnq]], [[1w72|1w72]], [[2jcc|2jcc]], [[2bck|2bck]], [[1de4|1de4]], [[2vlk|2vlk]], [[1exu|1exu]], [[1qrn|1qrn]], [[2hla|2hla]], [[1mhe|1mhe]], [[1eez|1eez]], [[1im9|1im9]], [[1jht|1jht]], [[1qqd|1qqd]], [[1qr1|1qr1]], [[1zs8|1zs8]], [[1hla|1hla]], [[1jgd|1jgd]], [[1i1y|1i1y]], [[1vgk|1vgk]], [[1age|1age]], [[1ur7|1ur7]], [[2x89|2x89]], [[1s9x|1s9x]], [[1hhg|1hhg]], [[2x4u|2x4u]], [[1duz|1duz]], [[1a9e|1a9e]], [[2clr|2clr]], [[3hla|3hla]], [[1m05|1m05]], [[2x4o|2x4o]], [[1tvb|1tvb]], [[2v2w|2v2w]], [[1onq|1onq]], [[2x4p|2x4p]], [[2vlr|2vlr]], [[2bvo|2bvo]], [[1a1n|1a1n]], [[1lp9|1lp9]], [[1zsd|1zsd]], [[1m6o|1m6o]], [[1hhk|1hhk]], [[1zt4|1zt4]], [[1hsb|1hsb]], [[1ce6|1ce6]], [[2xku|2xku]], [[1x7q|1x7q]], [[1py4|1py4]], [[1syv|1syv]], [[2j8u|2j8u]], [[1sys|1sys]], [[1ogt|1ogt]], [[2x4t|2x4t]], [[1cg9|1cg9]], [[1p7q|1p7q]], [[1q94|1q94]], [[1jnj|1jnj]], [[1agb|1agb]], [[2d31|2d31]], [[1xz0|1xz0]], [[1lds|1lds]], [[1hhh|1hhh]], [[1tvh|1tvh]], [[1xr8|1xr8]], [[2bss|2bss]], [[1a1m|1a1m]], [[1e28|1e28]], [[2bvp|2bvp]], [[2v2x|2v2x]], [[1xr9|1xr9]], [[2gj6|2gj6]], [[2x4r|2x4r]], [[1qlf|1qlf]], [[1efx|1efx]], [[1tmc|1tmc]], [[2av1|2av1]], [[1qsf|1qsf]], [[1jge|1jge]], [[1kpr|1kpr]], [[1duy|1duy]], [[2hjl|2hjl]], [[1qew|1qew]], [[1w0v|1w0v]], [[1k5n|1k5n]], [[1ao7|1ao7]], [[2bnr|2bnr]], [[1xh3|1xh3]], [[2bst|2bst]], [[1mi5|1mi5]], [[2h26|2h26]], [[1s9y|1s9y]], [[1a1o|1a1o]], [[2a83|2a83]], [[1agf|1agf]], [[1oga|1oga]], [[2f8o|2f8o]], [[2x70|2x70]], [[2cii|2cii]], [[1i7r|1i7r]], [[1jf1|1jf1]], [[2c7u|2c7u]], [[2f74|2f74]], [[1e27|1e27]], [[1w0w|1w0w]], [[1gzq|1gzq]], [[1uxs|1uxs]], [[1akj|1akj]], [[2hjk|2hjk]], [[2vb5|2vb5]], [[1agd|1agd]], [[2x4n|2x4n]], [[1r3h|1r3h]], [[1eey|1eey]], [[1i7t|1i7t]], [[1ydp|1ydp]], [[1i4f|1i4f]], [[2vll|2vll]], [[2bsr|2bsr]], [[1b0g|1b0g]], [[2vlj|2vlj]], [[2x4s|2x4s]], [[1b0r|1b0r]], [[1of2|1of2]], [[1hhi|1hhi]], [[1qse|1qse]], [[1a9b|1a9b]], [[2axg|2axg]], [[2bvq|2bvq]], [[1agc|1agc]], [[1qvo|1qvo]], [[1hhj|1hhj]], [[1s9w|1s9w]], [[1ktl|1ktl]], [[1a6z|1a6z]], [[2cik|2cik]], [[1i1f|1i1f]], [[2uwe|2uwe]], [[2av7|2av7]]</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2xpg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2xpg OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2xpg RCSB], [http://www.ebi.ac.uk/pdbsum/2xpg PDBsum]</span></td></tr>
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</table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/MYPR_HUMAN MYPR_HUMAN]] Defects in PLP1 are the cause of leukodystrophy hypomyelinating type 1 (HLD1) [MIM:[http://omim.org/entry/312080 312080]]; also known as Pelizaeus-Merzbacher disease. HLD1 is an X-linked recessive dysmyelinating disorder of the central nervous system in which myelin is not formed properly. It is characterized clinically by nystagmus, spastic quadriplegia, ataxia, and developmental delay.<ref>PMID:2479017</ref> <ref>PMID:2773936</ref> <ref>PMID:2480601</ref> <ref>PMID:1708672</ref> <ref>PMID:1707231</ref> <ref>PMID:1715570</ref> <ref>PMID:1376966</ref> <ref>PMID:1384324</ref> <ref>PMID:7684886</ref> <ref>PMID:7679906</ref> <ref>PMID:7683951</ref> <ref>PMID:8037216</ref> <ref>PMID:7539213</ref> <ref>PMID:7573159</ref> <ref>PMID:7541731</ref> <ref>PMID:7531827</ref> <ref>PMID:8909455</ref> <ref>PMID:9143933</ref> <ref>PMID:9008538</ref> <ref>PMID:9482656</ref> <ref>PMID:9788732</ref> <ref>PMID:9747038</ref> <ref>PMID:9633722</ref> <ref>PMID:10417279</ref> <ref>PMID:9934976</ref> <ref>PMID:9894878</ref> <ref>PMID:10425042</ref> <ref>PMID:11093273</ref> <ref>PMID:11786921</ref> <ref>PMID:15712223</ref> Defects in PLP1 are the cause of spastic paraplegia X-linked type 2 (SPG2) [MIM:[http://omim.org/entry/312920 312920]]. SPG2 is characterized by spastic gait and hyperreflexia. In some patients, complicating features include nystagmus, dysarthria, sensory disturbance, mental retardation, optic atrophy.<ref>PMID:11093273</ref> <ref>PMID:8012387</ref> <ref>PMID:7522741</ref> <ref>PMID:8956049</ref> <ref>PMID:8780101</ref> <ref>PMID:9489796</ref> <ref>PMID:10319897</ref> <ref>PMID:15450775</ref> <ref>PMID:17438221</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>
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== Function ==
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[[http://www.uniprot.org/uniprot/1A03_HUMAN 1A03_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/MYPR_HUMAN MYPR_HUMAN]] This is the major myelin protein from the central nervous system. It plays an important role in the formation or maintenance of the multilamellar structure of myelin. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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The structure of the human major histocompatability (MHC) class I molecule HLA-A*0301 (HLA-A3) in complex with a nonameric peptide (KLIETYFSK) has been determined by X-ray crystallography to 2.7 A resolution. HLA-A3 is a predisposing allele for multiple sclerosis (MS), an autoimmune disease of the central nervous system. The KLIETYFSK peptide is a naturally processed epitope of proteolipid protein, a myelin protein and candidate target for immune-mediated myelin destruction in MS. Comparison of the structure of HLA-A3 with that of HLA-A2, an MHC class I molecule which is protective against MS, indicates that both MHC class I molecules present very similar faces for T-cell receptor recognition whilst differing in the specificity of their peptide-binding grooves. These characteristics may underlie the opposing (predisposing versus protective) associations that they exhibit both in humans and in mouse models of MS-like disease. Furthermore, subtle alterations within the peptide-binding groove of HLA-A3 and other A3-like MHC class I molecules, members of the so-called A3 superfamily, may be sufficient to alter their presentation of autoantigen peptides such as KLIETYFSK. This in turn may modulate their contribution to the associated risk of autoimmune disease.
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==Disease==
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Structure of HLA-A*0301 in complex with a peptide of proteolipid protein: insights into the role of HLA-A alleles in susceptibility to multiple sclerosis.,McMahon RM, Friis L, Siebold C, Friese MA, Fugger L, Jones EY Acta Crystallogr D Biol Crystallogr. 2011 May;67(Pt 5):447-54. Epub 2011 Apr 13. PMID:21543847<ref>PMID:21543847</ref>
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[[http://www.uniprot.org/uniprot/MYPR_HUMAN MYPR_HUMAN]] Defects in PLP1 are the cause of leukodystrophy hypomyelinating type 1 (HLD1) [MIM:[http://omim.org/entry/312080 312080]]; also known as Pelizaeus-Merzbacher disease. HLD1 is an X-linked recessive dysmyelinating disorder of the central nervous system in which myelin is not formed properly. It is characterized clinically by nystagmus, spastic quadriplegia, ataxia, and developmental delay.<ref>PMID:2479017</ref><ref>PMID:2773936</ref><ref>PMID:2480601</ref><ref>PMID:1708672</ref><ref>PMID:1707231</ref><ref>PMID:1715570</ref><ref>PMID:1376966</ref><ref>PMID:1384324</ref><ref>PMID:7684886</ref><ref>PMID:7679906</ref><ref>PMID:7683951</ref><ref>PMID:8037216</ref><ref>PMID:7539213</ref><ref>PMID:7573159</ref><ref>PMID:7541731</ref><ref>PMID:7531827</ref><ref>PMID:8909455</ref><ref>PMID:9143933</ref><ref>PMID:9008538</ref><ref>PMID:9482656</ref><ref>PMID:9788732</ref><ref>PMID:9747038</ref><ref>PMID:9633722</ref><ref>PMID:10417279</ref><ref>PMID:9934976</ref><ref>PMID:9894878</ref><ref>PMID:10425042</ref><ref>PMID:11093273</ref><ref>PMID:11786921</ref><ref>PMID:15712223</ref> Defects in PLP1 are the cause of spastic paraplegia X-linked type 2 (SPG2) [MIM:[http://omim.org/entry/312920 312920]]. SPG2 is characterized by spastic gait and hyperreflexia. In some patients, complicating features include nystagmus, dysarthria, sensory disturbance, mental retardation, optic atrophy.<ref>PMID:11093273</ref><ref>PMID:8012387</ref><ref>PMID:7522741</ref><ref>PMID:8956049</ref><ref>PMID:8780101</ref><ref>PMID:9489796</ref><ref>PMID:10319897</ref><ref>PMID:15450775</ref><ref>PMID:17438221</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref><ref>PMID:1336137</ref><ref>PMID:7554280</ref><ref>PMID:4586824</ref><ref>PMID:8084451</ref><ref>PMID:12119416</ref><ref>PMID:12796775</ref><ref>PMID:16901902</ref><ref>PMID:16491088</ref><ref>PMID:17646174</ref><ref>PMID:18835253</ref><ref>PMID:18395224</ref><ref>PMID:19284997</ref>
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==Function==
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[http://www.uniprot.org/uniprot/1A03_HUMAN 1A03_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/MYPR_HUMAN MYPR_HUMAN]] This is the major myelin protein from the central nervous system. It plays an important role in the formation or maintenance of the multilamellar structure of myelin. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
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</div>
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==About this Structure==
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[[2xpg]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2XPG OCA].
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==See Also==
==See Also==
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*[[Major histocompatibility complex|Major histocompatibility complex]]
*[[Major histocompatibility complex|Major histocompatibility complex]]
*[[Multiple sclerosis|Multiple sclerosis]]
*[[Multiple sclerosis|Multiple sclerosis]]
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== References ==
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==Reference==
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<references/>
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<ref group="xtra">PMID:021543847</ref><references group="xtra"/><references/>
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__TOC__
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</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Friese, M A.]]
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[[Category: Friese, M A]]
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[[Category: Friis, L.]]
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[[Category: Friis, L]]
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[[Category: Fugger, L.]]
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[[Category: Fugger, L]]
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[[Category: Jones, E Y.]]
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[[Category: Jones, E Y]]
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[[Category: Mcmahon, R M.]]
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[[Category: Mcmahon, R M]]
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[[Category: Siebold, C.]]
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[[Category: Siebold, C]]
[[Category: Autoimmunity]]
[[Category: Autoimmunity]]
[[Category: Immune system]]
[[Category: Immune system]]
[[Category: Multiple sclerosis]]
[[Category: Multiple sclerosis]]

Revision as of 11:53, 18 December 2014

Crystal structure of a MHC class I-peptide complex

2xpg, resolution 2.60Å

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