3mv7: Difference between revisions
New page: '''Unreleased structure''' The entry 3mv7 is ON HOLD Authors: Gras, Stephanie, Chen, Zhenjun, Miles, John J., Liu, Yu C., Bell, Melissa J., Sullivan, Lucy C., Kjer-Nielsen, Lars, Brenna... |
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The | ==Crystal Structure of the TK3 TCR in complex with HLA-B*3501/HPVG== | ||
<StructureSection load='3mv7' size='340' side='right' caption='[[3mv7]], [[Resolution|resolution]] 2.00Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[3mv7]] is a 5 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3MV7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MV7 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2fyy|2fyy]], [[3mv8|3mv8]], [[3mv9|3mv9]]</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 HUMAN]), B2M, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=3mv7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mv7 OCA], [http://pdbe.org/3mv7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3mv7 RCSB], [http://www.ebi.ac.uk/pdbsum/3mv7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3mv7 ProSAT]</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/1B35_HUMAN 1B35_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/EBNA1_EBVB9 EBNA1_EBVB9]] Plays an essential role in replication and partitioning of viral genomic DNA during latent viral infection. During this phase, the circular double-stranded viral DNA undergoes replication once per cell cycle and is efficiently partitioned to the daughter cells. EBNA1 activates the initiation of viral DNA replication through binding to specific sites in the viral latent origin of replication, oriP. Additionally, it governs the segregation of viral episomes by mediating their attachment to host cell metaphase chromosomes. Also activates the transcription of several viral latency genes. Finally, it can counteract the stabilization of host p53/TP53 by host USP7, thereby decreasing apoptosis and increasing host cell survival.<ref>PMID:15808506</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/mv/3mv7_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/main_output.php?pdb_ID=3mv7 ConSurf]. | |||
<div style="clear:both"></div> | |||
<div style="background-color:#fffaf0;"> | |||
== Publication Abstract from PubMed == | |||
In comparison to human leukocyte antigen (HLA) polymorphism, the impact of allelic sequence variation within T cell receptor (TCR) loci is much less understood. Particular TCR loci have been associated with autoimmunity, but the molecular basis for this phenomenon is undefined. We examined the T cell response to an HLA-B*3501-restricted epitope (HPVGEADYFEY) from Epstein-Barr virus (EBV), which is frequently dominated by a TRBV9*01(+) public TCR (TK3). However, the common allelic variant TRBV9*02, which differs by a single amino acid near the CDR2beta loop (Gln55-->His55), was never used in this response. The structure of the TK3 TCR, its allelic variant, and a nonnaturally occurring mutant (Gln55-->Ala55) in complex with HLA-B*3501(HPVGEADYFEY) revealed that the Gln55-->His55 polymorphism affected the charge complementarity at the TCR-peptide-MHC interface, resulting in reduced functional recognition of the cognate and naturally occurring variants of this EBV peptide. Thus, polymorphism in the TCR loci may contribute toward variability in immune responses and the outcome of infection. | |||
Allelic polymorphism in the T cell receptor and its impact on immune responses.,Gras S, Chen Z, Miles JJ, Liu YC, Bell MJ, Sullivan LC, Kjer-Nielsen L, Brennan RM, Burrows JM, Neller MA, Khanna R, Purcell AW, Brooks AG, McCluskey J, Rossjohn J, Burrows SR J Exp Med. 2010 Jul 5;207(7):1555-67. Epub 2010 Jun 21. PMID:20566715<ref>PMID:20566715</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
</div> | |||
<div class="pdbe-citations 3mv7" style="background-color:#fffaf0;"></div> | |||
==See Also== | |||
*[[Beta-2 microglobulin|Beta-2 microglobulin]] | |||
*[[Major histocompatibility complex|Major histocompatibility complex]] | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Human]] | |||
[[Category: Bell, M J]] | |||
[[Category: Brennan, R M]] | |||
[[Category: Brooks, A G]] | |||
[[Category: Burrows, J M]] | |||
[[Category: Burrows, S R]] | |||
[[Category: Chen, Z]] | |||
[[Category: Gras, S]] | |||
[[Category: Khanna, R]] | |||
[[Category: Kjer-Nielsen, L]] | |||
[[Category: Liu, Y C]] | |||
[[Category: McCluskey, J]] | |||
[[Category: Miles, J J]] | |||
[[Category: Neller, M A]] | |||
[[Category: Purcell, A W]] | |||
[[Category: Rossjohn, J]] | |||
[[Category: Sullivan, L C]] | |||
[[Category: Ebv]] | |||
[[Category: Hla b*3501]] | |||
[[Category: Hpvg]] | |||
[[Category: Immune system]] | |||
[[Category: Tcr]] | |||
[[Category: Tcr polymorphism]] | |||
[[Category: Tcrpmhc complex]] | |||