anti-UL16 Binding Protein 2 (ULBP2) 抗体

Human UL16 Binding Protein 2 (ULBP2) interaction partners

1. Data show that the response of NK cells activated by ULBP2 was augmented by an interaction between NKG2D ligand 2 protein (ULBP2)-bound natural killer group 2D (NKG2D) and IL- interleukin 15 receptor (IL-15R).

2. NK cells are important cytotoxic cells in the immune system, and the activated NKG2D receptor on the NK cell surface can bind to NKG2D ligands expressed in tumor cells, enabling NK cells to activate and kill tumor cells. (Review)

3. High ULBP2 expression is associated with lymphoma.

4. IMP3 directly interacts with ULBP2 mRNA, leading to ULBP2 transcript destabilization and reduced ULBP2 surface expression and indirectly downregulates MICB with a mechanism functionally distinct from that of ULBP2.

5. By suppressing AR and up-regulating ULBP2 in HCC, cisplatin could up-regulate cytotoxicity of NK cells to better target HCC.

6. human tumor cells lost their surface expression of ULBP2, but not ULBP1 and ULBP3, during NK cell-mediated cytolysis.

7. This study suggests that NKG2D ligands shedding of MICA, MICB and ULBP-2 is a novel pathway in endometriosis complex pathogenesis that impairs Natural Killer Cells cell function.

8. Varicella-Zoster Virus differentially modulates expression of the NKG2D ligands by upregulating MICA expression and reducing ULBP2 and ULBP3 expression in the infected cells.

9. A conserved WW domain-like motif regulates CD74 antigen-dependent cell-surface transport of the NKG2D ligand ULBP2.

10. NKG2D and NKG2DL are involved in allergen-induced activation of dendritic epidermal T cells and the NKG2D/NKG2DL pathway might be a potential target for treatment of contact hypersensitivity.

11. Human anaplastic thyroid carcinoma cells are sensitive to NK cell-mediated lysis via ULBP2/5/6 and chemoattract NK cells.

12. Data inticate that heat shock protein 60 (HSP60) interacted constitutively with NKG2D ligand ULBP2 and phosphatase of regenerating liver 3 (PRL-3) regulated HSP60 tyrosine phosphorylation.

13. Results suggest that ULBP2 is expressed and released from cervical cancer cells by CRF, which regulates NKG2D expression in natural killer cells.

14. c-Cbl regulates MICA- but not ULBP2-induced NKG2D down-modulation in human NK cells.

15. the NKG2D ligand ULBP2 is transported to the cell surface through an endosomal pathway dependent on protein kinase C and lysosomal integrity. ULBP2 surface transport is dependent on the invariant chain.

16. This study provides for the first time, the c-Myc dependent regulation of NKG2D ligands, ULBP1/2/3 in acute myeloid leukemia.

17. Vpr augments ULBP2 expression on both infected and uninfected bystander cells during HIV-1 infection of primary CD4+ T lymphocytes.

18. Study shows that tumor-suppressive miR-34a and miR-34c act as ULBP2 repressors. Findings also implicate p53 in ULBP2 regulation, emphasizing the role of the specific NKG2DL in tumor immune surveillance.

19. Data show that VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression.

20. Findings define the involvement of p53 in the regulation of ULBP1 and ULBP2 which enhance NK cell-mediated target recognition.