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{{STRUCTURE_3dx8| PDB=3dx8 | SCENE=  }}
==Crystal Structure of B*4405 presenting a 10mer EBV epitope==
===Crystal Structure of B*4405 presenting a 10mer EBV epitope===
<StructureSection load='3dx8' size='340' side='right' caption='[[3dx8]], [[Resolution|resolution]] 2.10&Aring;' scene=''>
{{ABSTRACT_PUBMED_19139173}}
== Structural highlights ==
<table><tr><td colspan='2'>[[3dx8]] 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=3DX8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3DX8 FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3dx6|3dx6]], [[3dx7|3dx7]], [[3dx9|3dx9]], [[3dxa|3dxa]]</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
<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=3dx8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3dx8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3dx8 RCSB], [http://www.ebi.ac.uk/pdbsum/3dx8 PDBsum]</span></td></tr>
</table>
== Disease ==
[[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>  
== Function ==
[[http://www.uniprot.org/uniprot/1B44_HUMAN 1B44_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/EBNA6_EBV EBNA6_EBV]] Plays an essential role for the activation and immortalization of human B-cells. Represses transcription of viral promoters TP1 and Cp through interaction with host RBPJ, and inhibits EBNA2-mediated activation of these promoters. Since Cp is the promoter for all EBNA mRNAs, EBNA6 probably contributes to a negative autoregulatory control loop. Alternatively, EBNA6 also regulates the transcription of the EBV oncogene LMP1 in a cell cycle-dependent manner. It modulates the activity of several host proteins involved in cell cycle regulation including host cyclin A, MYC, RB and p27 mainly through binding to the host SCF(SKP2) complex.<ref>PMID:16352731</ref>  [[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.
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
  <jmolCheckbox>
    <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/dx/3dx8_consurf.spt"</scriptWhenChecked>
    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
    <text>to colour the structure by Evolutionary Conservation</text>
  </jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
Human leukocyte antigen (HLA) gene polymorphism plays a critical role in protective immunity, disease susceptibility, autoimmunity, and drug hypersensitivity, yet the basis of how HLA polymorphism influences T cell receptor (TCR) recognition is unclear. We examined how a natural micropolymorphism in HLA-B44, an important and large HLA allelic family, affected antigen recognition. T cell-mediated immunity to an Epstein-Barr virus determinant (EENLLDFVRF) is enhanced when HLA-B*4405 was the presenting allotype compared with HLA-B*4402 or HLA-B*4403, each of which differ by just one amino acid. The micropolymorphism in these HLA-B44 allotypes altered the mode of binding and dynamics of the bound viral epitope. The structure of the TCR-HLA-B*4405(EENLLDFVRF) complex revealed that peptide flexibility was a critical parameter in enabling preferential engagement with HLA-B*4405 in comparison to HLA-B*4402/03. Accordingly, major histocompatibility complex (MHC) polymorphism can alter the dynamics of the peptide-MHC landscape, resulting in fine-tuning of T cell responses between closely related allotypes.


==Disease==
Natural micropolymorphism in human leukocyte antigens provides a basis for genetic control of antigen recognition.,Archbold JK, Macdonald WA, Gras S, Ely LK, Miles JJ, Bell MJ, Brennan RM, Beddoe T, Wilce MC, Clements CS, Purcell AW, McCluskey J, Burrows SR, Rossjohn J J Exp Med. 2009 Jan 16;206(1):209-19. Epub 2009 Jan 12. PMID:19139173<ref>PMID:19139173</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>  


==Function==
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
[[http://www.uniprot.org/uniprot/1B44_HUMAN 1B44_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/EBNA6_EBV EBNA6_EBV]] Plays an essential role for the activation and immortalization of human B-cells. Represses transcription of viral promoters TP1 and Cp through interaction with host RBPJ, and inhibits EBNA2-mediated activation of these promoters. Since Cp is the promoter for all EBNA mRNAs, EBNA6 probably contributes to a negative autoregulatory control loop. Alternatively, EBNA6 also regulates the transcription of the EBV oncogene LMP1 in a cell cycle-dependent manner. It modulates the activity of several host proteins involved in cell cycle regulation including host cyclin A, MYC, RB and p27 mainly through binding to the host SCF(SKP2) complex.<ref>PMID:16352731</ref> [[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.
</div>
 
==About this Structure==
[[3dx8]] 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=3DX8 OCA].


==See Also==
==See Also==
*[[Beta-2 microglobulin|Beta-2 microglobulin]]
*[[Beta-2 microglobulin|Beta-2 microglobulin]]
*[[Major histocompatibility complex|Major histocompatibility complex]]
*[[Major histocompatibility complex|Major histocompatibility complex]]
 
== References ==
==Reference==
<references/>
<ref group="xtra">PMID:019139173</ref><references group="xtra"/><references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Archbold, J K.]]
[[Category: Archbold, J K]]
[[Category: Ely, L K.]]
[[Category: Ely, L K]]
[[Category: Rossjohn, J.]]
[[Category: Rossjohn, J]]
[[Category: Disease mutation]]
[[Category: Disease mutation]]
[[Category: Glycation]]
[[Category: Glycation]]

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