anti-CLEC2D (CLEC2D) Antikörper

Human C-Type Lectin Domain Family 2, Member D (CLEC2D) Interaktionspartner

1. Blocking LLT1-NKRP1A (zeige KLRB1 Antikörper) interaction will make prostate cancer cells susceptible to killing by NK cells, suggesting a therapeutic option for treatment of prostate cancer.

2. these data suggest that LLT1-CD161 (zeige KLRB1 Antikörper) interactions play a novel and important role in B cell maturation (zeige TNFRSF17 Antikörper) within the Germinal center in humans.

3. In RA joints, LLT1 is expressed by cells of the monocyte/macrophage lineage.

4. The hexamer of glycosylated LLT1 consists of three classical dimers. The hexameric packing may indicate a possible mode of interaction of C-type lectin (zeige MBL2 Antikörper)-like proteins in the glycosylated form.

5. One polymorphism in LLT1 was found to be associated with our Crohn's Disease population (P<0.034).Our Ulcerative Colitis cohort was not associated with the variation in LLT1 (P=0.33)

6. LLT1 and CD161 (zeige KLRB1 Antikörper) have roles in modulating immune responses to pathogens; and interferon-gamma (zeige IFNG Antikörper) contributes to modulate immune responses

7. Molecular basis for LLT1 protein recognition by human CD161 (zeige KLRB1 Antikörper) protein (NKRP1A/KLRB1 (zeige KLRB1 Antikörper)).

8. Data show that only CLEC2D isoform 1 (LLT1) is expressed on the cell surface.

9. LLT1 used Src (zeige SRC Antikörper)-PTK, p38 (zeige CRK Antikörper) and ERK (zeige EPHB2 Antikörper) signalling pathways, but not PKC (zeige PRRT2 Antikörper), PI3K (zeige PIK3CA Antikörper) or calcineurin pathways, to increase production of IFN-gamma (zeige IFNG Antikörper) by human natural killer cells.

10. LLT1 induces Interferon (zeige IFNA Antikörper) Type II production by natural killer cells.

Mouse (Murine) C-Type Lectin Domain Family 2, Member D (CLEC2D) Interaktionspartner

1. these findings demonstrate that Clr-b is an IFN-stimulated gene on healthy bystander cells, in addition to a missing-self marker on MCMV-infected cells, and thereby enhances the dynamic range of innate self-nonself discrimination by NK cells

2. Data suggest that killer cell lectin-like receptors NKR (zeige TACR3 Antikörper)-P1B:Clr-b (Klrb1 (zeige KLRB1 Antikörper):Clec2d) interactions may provide a model for human hematopoietic cell transplants.

3. Reductions of Clr-b may be involved in sensitizing poxvirus-infected cells to natural killer (NK) cells.

4. LLT1 and CD161 have roles in modulating immune responses to pathogens; and interferon-gamma (zeige IFNG Antikörper) contributes to modulate immune responses

5. cloning and characterization of a cognate ligand, Ocil, for the inhibitory NK receptors (NKR)-P1B and NKR-P1D. Ocil/Clr-b is displayed at high levels on nearly all hematopoietic cells, in a pattern that is similar to that of class I MHC molecules.

6. Data show that osteoclast inhibitory lectin (OCIL) binds a range of physiologically important glycosaminoglycans, and this property may modulate OCIL actions upon other cells.

7. Limited divergence of the BALB/c Nkrp1-Ocil/Clr region helps explain a longstanding confusion regarding the strain-specific NK1.1 alloantigen reactivity of mouse natural killer cells.

8. OCIL is a physiological negative regulator of bone.

9. PTHrp(1-34) regulates OCIL expression in vitro through cAMP/PKA, Ca(2 (zeige CA2 Antikörper)+)/CaMK II (zeige CAMK2B Antikörper), and MAPK (zeige MAPK1 Antikörper) signaling pathways.

10. Identification of a novel family of genes, named Clr (zeige CALCR Antikörper), encoding C-type lectin-like molecules, which maps in the natural killer (NK) gene complex (NKC) on mouse Chromosome 6.