3o4l
From Proteopedia
(Difference between revisions)
| Line 1: | Line 1: | ||
| - | + | ==Genetic and structural basis for selection of a ubiquitous T cell receptor deployed in Epstein-Barr virus== | |
| - | + | <StructureSection load='3o4l' size='340' side='right' caption='[[3o4l]], [[Resolution|resolution]] 2.54Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[3o4l]] is a 5 chain structure with sequence from [http://en.wikipedia.org/wiki/Ebvg Ebvg] and [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3O4L OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3O4L FirstGlance]. <br> | |
| - | ==Disease== | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MES:2-(N-MORPHOLINO)-ETHANESULFONIC+ACID'>MES</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></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=3o4l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3o4l OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3o4l RCSB], [http://www.ebi.ac.uk/pdbsum/3o4l 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> | [[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 == | |
| - | ==Function== | + | |
[[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. | [[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 style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | Despite the approximately 10(18) alphabeta T cell receptor (TCR) structures that can be randomly manufactured by the human thymus, some surface more frequently than others. The pinnacles of this distortion are public TCRs, which exhibit amino acid-identical structures across different individuals. Public TCRs are thought to result from both recombinatorial bias and antigen-driven selection, but the mechanisms that underlie inter-individual TCR sharing are still largely theoretical. To examine this phenomenon at the atomic level, we solved the co-complex structure of one of the most widespread and numerically frequent public TCRs in the human population. The archetypal AS01 public TCR recognizes an immunodominant BMLF1 peptide, derived from the ubiquitous Epstein-Barr virus, bound to HLA-A*0201. The AS01 TCR was observed to dock in a diagonal fashion, grasping the solvent exposed peptide crest with two sets of complementarity-determining region (CDR) loops, and was fastened to the peptide and HLA-A*0201 platform with residue sets found only within TCR genes biased in the public response. Computer simulations of a random V(D)J recombination process demonstrated that both TCRalpha and TCRbeta amino acid sequences could be manufactured easily, thereby explaining the prevalence of this receptor across different individuals. Interestingly, the AS01 TCR was encoded largely by germline DNA, indicating that the TCR loci already comprise gene segments that specifically recognize this ancient pathogen. Such pattern recognition receptor-like traits within the alphabeta TCR system further blur the boundaries between the adaptive and innate immune systems. | ||
| - | + | Genetic and structural basis for selection of a ubiquitous T cell receptor deployed in Epstein-Barr virus infection.,Miles JJ, Bulek AM, Cole DK, Gostick E, Schauenburg AJ, Dolton G, Venturi V, Davenport MP, Tan MP, Burrows SR, Wooldridge L, Price DA, Rizkallah PJ, Sewell AK PLoS Pathog. 2010 Nov 18;6(11):e1001198. PMID:21124993<ref>PMID:21124993</ref> | |
| - | + | ||
| + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
| + | </div> | ||
==See Also== | ==See Also== | ||
*[[Beta-2 microglobulin|Beta-2 microglobulin]] | *[[Beta-2 microglobulin|Beta-2 microglobulin]] | ||
*[[T-cell receptor|T-cell receptor]] | *[[T-cell receptor|T-cell receptor]] | ||
| - | + | == References == | |
| - | == | + | <references/> |
| - | + | __TOC__ | |
| + | </StructureSection> | ||
[[Category: Ebvg]] | [[Category: Ebvg]] | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Bulek, A M | + | [[Category: Bulek, A M]] |
| - | [[Category: Burrows, S R | + | [[Category: Burrows, S R]] |
| - | [[Category: Cole, D K | + | [[Category: Cole, D K]] |
| - | [[Category: Davenport, M P | + | [[Category: Davenport, M P]] |
| - | [[Category: Dolton, G | + | [[Category: Dolton, G]] |
| - | [[Category: Gostick, E | + | [[Category: Gostick, E]] |
| - | [[Category: Miles, J J | + | [[Category: Miles, J J]] |
| - | [[Category: Price, D A | + | [[Category: Price, D A]] |
| - | [[Category: Rizkallah, P J | + | [[Category: Rizkallah, P J]] |
| - | [[Category: Schauenburg, J A | + | [[Category: Schauenburg, J A]] |
| - | [[Category: Sewell, A K | + | [[Category: Sewell, A K]] |
| - | [[Category: Tan, M P | + | [[Category: Tan, M P]] |
| - | [[Category: Venturi, V | + | [[Category: Venturi, V]] |
| - | [[Category: Wooldridge, L | + | [[Category: Wooldridge, L]] |
[[Category: Antigen presentation]] | [[Category: Antigen presentation]] | ||
[[Category: Immune recognition]] | [[Category: Immune recognition]] | ||
Revision as of 17:45, 21 December 2014
Genetic and structural basis for selection of a ubiquitous T cell receptor deployed in Epstein-Barr virus
| |||||||||||
Categories: Ebvg | Homo sapiens | Bulek, A M | Burrows, S R | Cole, D K | Davenport, M P | Dolton, G | Gostick, E | Miles, J J | Price, D A | Rizkallah, P J | Schauenburg, J A | Sewell, A K | Tan, M P | Venturi, V | Wooldridge, L | Antigen presentation | Immune recognition | Immune system | Immunoglobulin | Mhc i
