8tm0: Difference between revisions
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==Preclinical Characterization of Pan-NKG2D Ligand-Binding NKG2D Receptor Decoys== | |||
<StructureSection load='8tm0' size='340' side='right'caption='[[8tm0]], [[Resolution|resolution]] 3.83Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[8tm0]] is a 2 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=8TM0 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8TM0 FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.83Å</td></tr> | |||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></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=8tm0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8tm0 OCA], [https://pdbe.org/8tm0 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8tm0 RCSB], [https://www.ebi.ac.uk/pdbsum/8tm0 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8tm0 ProSAT]</span></td></tr> | |||
</table> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/NKG2D_HUMAN NKG2D_HUMAN] Receptor for MICA, MICB, ULBP1, ULBP2, ULBP3 (ULBP2>ULBP1>ULBP3) and ULBP4. Plays a role as a receptor for the recognition of MHC class I HLA-E molecules by NK cells and some cytotoxic T-cells. Involved in the immune surveillance exerted by T- and B-lymphocytes. | |||
<div style="background-color:#fffaf0;"> | |||
== Publication Abstract from PubMed == | |||
NKG2D and its ligands are critical regulators of protective immune responses controlling infections and cancer, defining a crucial immune signaling axis. Current therapeutic efforts targeting this axis almost exclusively aim at enhancing NKG2D-mediated effector functions. However, this axis can drive disease processes when dysregulated, in particular, driving stem-like cancer cell reprogramming and tumorigenesis through receptor/ligand self-stimulation on tumor cells. Despite complexities with its structure and biology, we developed multiple novel engineered proteins that functionally serve as axis-blocking NKG2D "decoys" and report biochemical, structural, in vitro, and in vivo evaluation of their functionality. | |||
Preclinical characterization of Pan-NKG2D ligand-binding NKG2D receptor decoys.,Rupert PB, Buerger M, Girard EJ, Frutoso M, Parrilla D, Ng K, Gooley T, Groh V, Strong RK Heliyon. 2024 Mar 27;10(7):e28583. doi: 10.1016/j.heliyon.2024.e28583. , eCollection 2024 Apr 15. PMID:38586421<ref>PMID:38586421</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
[[Category: | </div> | ||
[[Category: Rupert | <div class="pdbe-citations 8tm0" style="background-color:#fffaf0;"></div> | ||
[[Category: Strong | == References == | ||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Rupert PB]] | |||
[[Category: Strong R]] | |||