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Ligand for the NKG2D receptor, together with at least ULBP2 and ULBP3. Additionally we are shipping ULBP1 Antibodies (38) and ULBP1 Kits (12) and many more products for this protein.
Showing 10 out of 12 products:
ATF4 (show ATF4 Proteins) drives ULBP1 gene expression in cancer cell lines, while the RNA-binding protein (show PTBP1 Proteins) RBM4 (show RBM4 Proteins) supports ULBP1 expression by suppressing a novel alternatively spliced isoform of ULBP1 mRNA.
expression determines intrinsic acute myeloid leukemia (show BCL11A Proteins) susceptibility to allogeneic V[gamma]9V[delta]2 T cells
This study provides for the first time, the c-Myc (show MYC Proteins) dependent regulation of NKG2D (show KLRK1 Proteins) ligands, ULBP1/2/3 in acute myeloid leukemia (show BCL11A Proteins).
recurrence-free survival of patients with ULBP1-negative hepatocellular carcinoma (HCC (show FAM126A Proteins)) was significantly shorter than that of patients with ULBP1-positive HCC (show FAM126A Proteins)
Findings define the involvement of p53 (show TP53 Proteins) in the regulation of ULBP1 and ULBP2 (show ULBP2 Proteins) which enhance NK cell-mediated target recognition.
recombinant ULBP1 fused to CD45 (show PTPRC Proteins) 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 (show TFR2 Proteins) and IFITM1 (show IFITM1 Proteins) 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 Proteins) ligand, ULBP1 are expressed on immature dendritic cells and plays an important role in the cytotoxic effect of NK cells against iDC (show LMNA Proteins).
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 Proteins) receptor play a role in control of lymphomas, and that selection of NKG2D (show KLRK1 Proteins)-ligand (MULT1) loss mutants provides a mechanism for tumor escape.
An increased expression of the NKG2D (show KLRK1 Proteins) ligand MICA (show MICA Proteins) in systemic lupus erthematosus (SLE) patients' kidneys and Rae-1 (show RAE1 Proteins) 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 Proteins) with high affinity. (MULT1)
Mouse cytomegalovirus (MCMV) molecule fcr-1 promotes a rapid down-regulation of NKG2D (show KLRK1 Proteins) 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 Proteins) NKG2D (show KLRK1 Proteins); 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