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6vqo

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==T cell receptor-p53-HLA-A2 complex==
==T cell receptor-p53-HLA-A2 complex==
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<StructureSection load='6vqo' size='340' side='right'caption='[[6vqo]]' scene=''>
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<StructureSection load='6vqo' size='340' side='right'caption='[[6vqo]], [[Resolution|resolution]] 3.00&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6VQO OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6VQO FirstGlance]. <br>
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<table><tr><td colspan='2'>[[6vqo]] is a 10 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=6VQO OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6VQO FirstGlance]. <br>
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</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6vqo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6vqo OCA], [http://pdbe.org/6vqo PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6vqo RCSB], [http://www.ebi.ac.uk/pdbsum/6vqo PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6vqo ProSAT]</span></td></tr>
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</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HLA-A ([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>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6vqo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6vqo OCA], [http://pdbe.org/6vqo PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6vqo RCSB], [http://www.ebi.ac.uk/pdbsum/6vqo PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6vqo ProSAT]</span></td></tr>
</table>
</table>
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== Disease ==
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[[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/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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Adoptive cell therapy (ACT) with tumor-specific T cells can mediate cancer regression. The main target of tumor-specific T cells are neoantigens arising from mutations in self-proteins. Although the majority of cancer neoantigens are unique to each patient, and therefore not broadly useful for ACT, some are shared. We studied oligoclonal T-cell receptors (TCRs) that recognize a shared neoepitope arising from a driver mutation in the p53 oncogene (p53R175H) presented by HLA-A2. Here we report structures of wild-type and mutant p53-HLA-A2 ligands, as well as structures of three tumor-specific TCRs bound to p53R175H-HLA-A2. These structures reveal how a driver mutation in p53 rendered a self-peptide visible to T cells. The TCRs employ structurally distinct strategies that are highly focused on the mutation to discriminate between mutant and wild-type p53. The TCR-p53R175H-HLA-A2 complexes provide a framework for designing TCRs to improve potency for ACT without sacrificing specificity.
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Structural basis for oligoclonal T cell recognition of a shared p53 cancer neoantigen.,Wu D, Gallagher DT, Gowthaman R, Pierce BG, Mariuzza RA Nat Commun. 2020 Jun 9;11(1):2908. doi: 10.1038/s41467-020-16755-y. PMID:32518267<ref>PMID:32518267</ref>
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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</div>
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<div class="pdbe-citations 6vqo" style="background-color:#fffaf0;"></div>
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== References ==
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<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
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[[Category: Human]]
[[Category: Large Structures]]
[[Category: Large Structures]]
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[[Category: Gallagher DT]]
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[[Category: Gallagher, D T]]
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[[Category: Mariuzza RA]]
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[[Category: Mariuzza, R A]]
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[[Category: Pierce BG]]
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[[Category: Pierce, B G]]
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[[Category: Wu D]]
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[[Category: Wu, D]]
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[[Category: Adoptive cell therapy]]
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[[Category: Hla]]
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[[Category: Immune system]]
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[[Category: Mhc]]
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[[Category: Tcr complex]]

Revision as of 07:07, 25 June 2020

T cell receptor-p53-HLA-A2 complex

PDB ID 6vqo

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