Hematopoietic Cell Signal Transducer (HCST) ELISA Kits

Human Hematopoietic Cell Signal Transducer (HCST) interaction partners

1. These results suggest that NKG2D (show KLRK1 ELISA Kits)-DAP10 endocytosis represents a means to decrease cell surface receptor abundance, as well as to control signaling outcome in cytotoxic lymphocytes.

2. findings indicate that the functional interaction between RAGE (show AGER ELISA Kits) and DAP10 coordinately regulates S100A8 (show S100A8 ELISA Kits)/A9-mediated survival and/or apoptotic response of keratinocytes

3. TGF-beta1 (show TGFB1 ELISA Kits) may reduce the expression of NKG2D (show KLRK1 ELISA Kits)/DAP10 and 2B4 (show CD244 ELISA Kits)/SAPin patients with hepatitis B.

4. HMBOX1 negatively regulates the expression of NKG2D (show KLRK1 ELISA Kits) and the activation of the NKG2D (show KLRK1 ELISA Kits)/DAP10 signaling pathway in NK cells.

5. Other gamma(c) cytokines act similarly to IL-2 (show IL2 ELISA Kits) in up-regulating DAP10 expression and NKG2D (show KLRK1 ELISA Kits)-DAP10 surface expression.

6. TGF-BETA1 (show TGFB1 ELISA Kits) down-modulates surface NKG2D (show KLRK1 ELISA Kits) expression by controlling the transcriptional and translational levels of DAP10.

7. A transgenic mouse model demonstrates that induction of tolerance in Ly49H-positive natural killer (NK) cells by chronic exposure to virus-encoded ligand m157 requires signaling through the Ly49H adaptor protein DAP12 (show TYROBP ELISA Kits), not the DAP10 adaptor protein.

8. NKG2D (show KLRK1 ELISA Kits)-DAP10 triggers human NK cell-mediated killing via a Syk (show SYK ELISA Kits)-independent regulatory pathway.

9. both activated and expanded CD8 (show CD8A ELISA Kits)+ T cells and NK cells use DAP10 for cytolysis

10. Downstream targets of DAP10 and DAP12 (show TYROBP ELISA Kits) are constitutively activated in large granular lymphocyte leukemia cells, and expression of dominant-negative DAP10 and DAP12 (show TYROBP ELISA Kits) dramatically reduces their lytic capacity.

Mouse (Murine) Hematopoietic Cell Signal Transducer (HCST) interaction partners

1. Adoptive transfer of murine T cells expressing a chimeric-PD1 (show PDCD1 ELISA Kits)-Dap10 receptor may induce a preferential cytokine profile and T-cell differentiation phenotype for anti-lymphoma therapies.

2. Rat and mouse CD94/NKG2C heterodimers bind efficiently to both DAP12 and DAP10; this binding is critically dependent on the transmembrane lysine residue of CD94.

3. contributes to CD8 (show CD8A ELISA Kits)(+) T cell-mediated cytotoxic effector mechanisms during Mycobacterium tuberculosis infection

4. demonstrate a previously uncharacterized interaction of SHIP1 with DAP12 that limits TREM2- and DAP12-dependent signaling and identify a mechanism through which SHIP1 regulates key ITAM-containing receptors by blocking the binding and activation of PI3K

5. selective associations with DAP10 determine stimulatory versus costimulatory activity of NKG2D (show KLRK1 ELISA Kits)

6. Differential requirements for Vav (show VAV1 ELISA Kits) proteins in DAP10- and ITAM-mediated NK cell cytotoxicity.

7. The importance of Fcgr3 (show CD16 ELISA Kits)/Cd3z (show CD247 ELISA Kits), Hcst, and Tyrobp (show TYROBP ELISA Kits) in the activation of NK cells in the uterus of pregnant mice is reported.

8. Review of immune reactions against syngeneic tumors reveals an important physiological role of DAP10 adapter protein (show GRB10 ELISA Kits) signaling in maintaining tolerance to self, by controlling the development and activation threshold of autoreactive T cells.

9. DAP10 signaling is involved in adjusting the activation threshold and generation of natural killer T cells and regulatory T cells to avoid autoreactivity, but it also modulates antitumor mechanisms.

10. improved rejection of B16 melanomas in DAP10-deficient mice

Cow (Bovine) Hematopoietic Cell Signal Transducer (HCST) interaction partners

Zebrafish Hematopoietic Cell Signal Transducer (HCST) interaction partners

1. The structure of the adaptor protein dap10 has been identified in the zebrafish genome.