High impact information on Hcst

• Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors [1].
• In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA [1].
• Modulation of NKG2D was mostly dependent on the YxxM motif of DAP10, the NKG2D-associated adaptor that activates phosphoinositide 3 kinase [2].
• Natural killer (NK) cells express multiple activating receptors that initiate signaling cascades through DAP10- or immunoreceptor tyrosine-based activation motif-containing adapters, including DAP12 and FcRgamma [3].
• Differential requirements for Vav proteins in DAP10- and ITAM-mediated NK cell cytotoxicity [3].

Anatomical context of Hcst

• Vav1 controls DAP10-mediated natural cytotoxicity by regulating actin and microtubule dynamics [4].

Associations of Hcst with chemical compounds

• Herein, we identify Vav1, a Rho GTPase guanine nucleotide exchange factor, as a critical signaling mediator downstream of DAP10 in NK cells [4].

Other interactions of Hcst

• Co-immunoprecipitation experiments to identify associated adaptor proteins revealed a 10-12-kDa protein associated with SIRPbeta1 that was tyrosine-phosphorylated after PMN stimulation and is not DAP10/12 or Fc receptor gamma chain [5].

References