6vr5

<table><tr><td colspan='2'>[[6vr5]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6VR5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6VR5 FirstGlance]. <br>

== Function ==

[https://www.uniprot.org/uniprot/A0A140T913_HUMAN A0A140T913_HUMAN]

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== Publication Abstract from PubMed ==

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.

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>

From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>

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== References ==

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[[Category: Homo sapiens]]