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ATF4 (show ATF4 ELISA Kits) drives ULBP1 gene expression in cancer cell lines, while the RNA-binding protein (show PTBP1 ELISA Kits) RBM4 (show RBM4 ELISA Kits) supports ULBP1 expression by suppressing a novel alternatively spliced isoform of ULBP1 mRNA.
expression determines intrinsic acute myeloid leukemia (show BCL11A ELISA Kits) susceptibility to allogeneic V[gamma]9V[delta]2 T cells
This study provides for the first time, the c-Myc (show MYC ELISA Kits) dependent regulation of NKG2D (show KLRK1 ELISA Kits) ligands, ULBP1/2/3 in acute myeloid leukemia (show BCL11A ELISA Kits).
recurrence-free survival of patients with ULBP1-negative hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) was significantly shorter than that of patients with ULBP1-positive HCC (show FAM126A ELISA Kits)
Findings define the involvement of p53 (show TP53 ELISA Kits) in the regulation of ULBP1 and ULBP2 (show ULBP2 ELISA Kits) which enhance NK cell-mediated target recognition.
recombinant ULBP1 fused to CD45 (show PTPRC ELISA Kits) 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 (show KLRK1 ELISA Kits) ligand, ULBP1 are expressed on immature dendritic cells and plays an important role in the cytotoxic effect of NK cells against iDC (show LMNA ELISA Kits).
Data show that the protease NS3/4A of HCV down-regulates ULBP1 expression by inhibiting the transcription of ULBP1.
The results show that NK cells and the NKG2D (show KLRK1 ELISA Kits) receptor play a role in control of lymphomas, and that selection of NKG2D (show KLRK1 ELISA Kits)-ligand (MULT1) loss mutants provides a mechanism for tumor escape.
An increased expression of the NKG2D (show KLRK1 ELISA Kits) ligand MICA (show MICA ELISA Kits) in systemic lupus erthematosus (SLE) patients' kidneys and Rae-1 (show RAE1 ELISA Kits) and Mult-1 in various murine SLE models, is reported.
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 (show KLRK1 ELISA Kits) with high affinity. (MULT1)
Mouse cytomegalovirus (MCMV) molecule fcr-1 promotes a rapid down-regulation of NKG2D (show KLRK1 ELISA Kits) 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 (show NCR1 ELISA Kits) NKG2D (show KLRK1 ELISA Kits); if eliminated on porcine tissues ULBP1 represents an attractive target to protect porcine xenografts from human NK cytotoxicity.
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.
UL16 binding protein 1
, NKG2D ligand 1
, UL16-binding protein 1
, retinoic acid early transcript 1I
, UL16-binding protein-like transcript 1
, NK cell receptor ligand