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we show that Simian Virus 40 (SV40)...evades NK cell attack through the down regulation of...ULBP1
ATF4 drives ULBP1 gene expression in cancer cell lines, while the RNA-binding protein RBM4 supports ULBP1 expression by suppressing a novel alternatively spliced isoform of ULBP1 mRNA.
expression determines intrinsic acute myeloid leukemia susceptibility to allogeneic V[gamma]9V[delta]2 T cells
This study provides for the first time, the c-Myc dependent regulation of NKG2D ligands, ULBP1/2/3 in acute myeloid leukemia.
recurrence-free survival of patients with ULBP1-negative hepatocellular carcinoma (HCC) was significantly shorter than that of patients with ULBP1-positive HCC
Findings define the involvement of p53 in the regulation of ULBP1 and ULBP2 which enhance NK cell-mediated target recognition.
recombinant ULBP1 fused to CD45 caused a reduction in cytotoxicity and degranulation by NK cells, implying a role for receptor ligand distribution in the activation of NK cell responses
Data show that ULBP1, TFR2 and IFITM1 were associated with increased susceptibility to Vgamma9Vdelta2 T-cell cytotoxicity.
These results identify Mult1 as a target for the MARCH family of E3 ligases
As NKG2D ligand, ULBP1 are expressed on immature dendritic cells and plays an important role in the cytotoxic effect of NK cells against iDC.
Data show that the protease NS3/4A of HCV down-regulates ULBP1 expression by inhibiting the transcription of ULBP1.
ULBP1 binds to the NKG2D receptor and activates multiple signaling pathways in primary natural killer cells.
The NKG2D ligand ULBP1 is up-regulated and readily detectable intracellularly in the endoplasmic reticulum of human cytomegalovirus-infected fibroblasts, where it colocalizes with viral protein UL16.
ULBPs and MICA are expressed in lipid rafts at the cell surface of NK and T cells.
ULBP1 is a human ligand of the NKG2D receptor
The selective induction of ULBP1 expression by proteasome inhibitor drugs, along with variable NKG2D ligand expression by human tumor cells, indicates that NKG2D ligand genes are independently regulated.
Vpr specifically induces surface expression of the unique-long 16 binding proteins (ULBP)-1 and ULBP-2, but not ULBP-3
The results show that NK cells and the NKG2D receptor play a role in control of lymphomas, and that selection of NKG2D-ligand (MULT1) loss mutants provides a mechanism for tumor escape.
An increased expression of the NKG2D ligand MICA in systemic lupus erthematosus (SLE) patients' kidneys and Rae-1 and Mult-1 in various murine SLE models, is reported.
Although the study is preliminary, the data suggest that the MULT1E/mIL-12 bi-functional fusion protein is an effective activator of NK cells for cancer treatment.
MULT1 (UL16-binding protein-like transcript 1) is expressed in adult parenchyma, possesses MHC class I-like alpha 1 and alpha 2 domains and a large cytoplasmic domain, and binds NKG2D with high affinity. (MULT1)
Mouse cytomegalovirus (MCMV) molecule fcr-1 promotes a rapid down-regulation of NKG2D ligands murine UL16-binding protein like transcript (MULT)-1 and H60 from the cell surface.
ULBP1 is the predominant, if not only, functional porcine ligand for human natural killer (NK) cell activating receptor NKG2D; if eliminated on porcine tissues ULBP1 represents an attractive target to protect porcine xenografts from human NK cytotoxicity.
Exposure of porcine aortic endothelial cells to hypoxia only slightly increased porcine UL-16 binding protein 1 expression
Ligand for the NKG2D receptor, together with at least ULBP2 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway. In CMV infected cells, interacts with soluble CMV glycoprotein UL16. The interaction with UL16 blocked the interaction with the NKG2D receptor, providing a mechanism by which CMV infected cells might escape the immune system. UL16 also causes ULBP1 to be retained in the ER and cis- Golgi apparatus so that it does not reach the cell surface.
, NKG2D ligand 1
, UL16-binding protein 1
, retinoic acid early transcript 1I
, UL16 binding protein 1
, UL16-binding protein-like transcript 1
, NK cell receptor ligand