7tr4
From Proteopedia
(Difference between revisions)
| Line 8: | Line 8: | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7tr4 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tr4 OCA], [https://pdbe.org/7tr4 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tr4 RCSB], [https://www.ebi.ac.uk/pdbsum/7tr4 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tr4 ProSAT]</span></td></tr> | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7tr4 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tr4 OCA], [https://pdbe.org/7tr4 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tr4 RCSB], [https://www.ebi.ac.uk/pdbsum/7tr4 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tr4 ProSAT]</span></td></tr> | ||
</table> | </table> | ||
| - | == Disease == | ||
| - | [https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[https://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 == | ||
| - | [https://www.uniprot.org/uniprot/ | + | [https://www.uniprot.org/uniprot/A0A140T9X5_HUMAN A0A140T9X5_HUMAN] |
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | Monoclonal antibodies (Abs) that recognize major histocompatability complex (MHC)-presented tumor antigens in a manner similar to T cell receptors (TCRs) have great potential as cancer immunotherapeutics. However, isolation of 'TCR-mimic' (TCRm) Abs is laborious because Abs have not evolved the structurally nuanced peptide-MHC restriction of alphabeta-TCRs. Here, we present a strategy for rapid isolation of highly peptide-specific and 'MHC-restricted' Abs by re-engineering preselected Abs that engage peptide-MHC in a manner structurally similar to that of conventional alphabeta-TCRs. We created structure-based libraries focused on the peptide-interacting residues of TCRm Ab complementarity-determining region (CDR) loops, and rapidly generated MHC-restricted Abs to both mouse and human tumor antigens that specifically killed target cells when formatted as IgG, bispecific T cell engager (BiTE) and chimeric antigen receptor-T (CAR-T). Crystallographic analysis of one selected pMHC-restricted Ab revealed highly peptide-specific recognition, validating the engineering strategy. This approach can yield tumor antigen-specific antibodies in several weeks, potentially enabling rapid clinical translation. | ||
| + | |||
| + | Facile repurposing of peptide-MHC-restricted antibodies for cancer immunotherapy.,Yang X, Nishimiya D, Lochte S, Jude KM, Borowska M, Savvides CS, Dougan M, Su L, Zhao X, Piehler J, Garcia KC Nat Biotechnol. 2023 Jul;41(7):932-943. doi: 10.1038/s41587-022-01567-w. Epub , 2023 Jan 2. PMID:36593402<ref>PMID:36593402</ref> | ||
| + | |||
| + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
| + | </div> | ||
| + | <div class="pdbe-citations 7tr4" style="background-color:#fffaf0;"></div> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Current revision
MA2-MART1-HLAA0201
| |||||||||||
