Abstract 875: Genetic variation in the natural killer cell activating receptor NKG2D and its ligands in relation to glioma risk and outcome

2011 ◽  
Author(s):  
James E. Browning ◽  
Reid C. Thompson ◽  
L. Burton Nabors ◽  
Jeffrey J. Olson ◽  
Melissa H. Madden ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Glioma Risk ◽  
Activating Receptor

scholarly journals Metalloprotease-Mediated Tumor Cell Shedding of B7-H6, the Ligand of the Natural Killer Cell–Activating Receptor NKp30

2014 ◽  
Vol 74 (13) ◽  
pp. 3429-3440 ◽  
Author(s):  
Eva Schlecker ◽  
Nathalie Fiegler ◽  
Annette Arnold ◽  
Peter Altevogt ◽  
Stefan Rose-John ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Tumor Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Cell Shedding ◽  
Activating Receptor

scholarly journals * Genetic variation in natural killer cell receptor protein G2D does not modify susceptibility to sporadic cholangiocarcinoma

Gut ◽  
2011 ◽  
Vol 60 (Suppl 1) ◽  
pp. A117-A117
Author(s):  
C. A. Wadsworth ◽  
P. H. Dixon ◽  
A. A. Zabron ◽  
J. H. Wong ◽  
M. H. Chapman ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Cell Receptor ◽  
Receptor Protein ◽  
Natural Killer Cell Receptor

scholarly journals Human cytomegalovirus UL141 promotes efficient downregulation of the natural killer cell activating ligand CD112

2010 ◽  
Vol 91 (8) ◽  
pp. 2034-2039 ◽  
Author(s):  
Virginie Prod'homme ◽  
Daniel M. Sugrue ◽  
Richard J. Stanton ◽  
Akio Nomoto ◽  
James Davies ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Human Cytomegalovirus ◽  
Killer Cell ◽  
Surface Expression ◽  
Productive Infection ◽  
Cell Surface Expression ◽  
Poliovirus Receptor ◽  
Activating Receptor

Human cytomegalovirus (HCMV) UL141 induces protection against natural killer cell-mediated cytolysis by downregulating cell surface expression of CD155 (nectin-like molecule 5; poliovirus receptor), a ligand for the activating receptor DNAM-1 (CD226). However, DNAM-1 is also recognized to bind a second ligand, CD112 (nectin-2). We now show that HCMV targets CD112 for proteasome-mediated degradation by 48 h post-infection, thus removing both activating ligands for DNAM-1 from the cell surface during productive infection. Significantly, cell surface expression of both CD112 and CD155 was restored when UL141 was deleted from the HCMV genome. While gpUL141 alone is sufficient to mediate retention of CD155 in the endoplasmic reticulum, UL141 requires assistance from additional HCMV-encoded functions to suppress expression of CD112.

Sign in / Sign up

Export Citation Format

Share Document