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== 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.

== 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>

</div>

== References ==

__TOC__

</StructureSection>

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 == 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&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
+</div>
+<div class="pdbe-citations 8tm0" style="background-color:#fffaf0;"></div>
+== References ==
+<references/>
 __TOC__
 </StructureSection>