-
Biochemical analyses revealed that mutant T cells were hypersensitive to TCR stimulation. Indeed, phosphorylation of several signaling proteins, including SLP76 itself, phospholipase Cgamma1 and the protein kinases AKT and ERK1/2, was increased
-
slp-76 contributes to the regulation of the tissue distribution, PLZF, and cytokine expression of iNKT cells via ADAP-dependent and -independent mechanisms.
-
findings identify ACK1 as a novel SLP-76-associated protein-tyrosine kinase that modulates early activation events in T cells.
-
immune cell adaptor SLP-76 binds directly to SUMO-RanGAP1 of cytoplasmic fibrils of the nuclear pore complex, and this interaction is needed for optimal NFATc1 and NF-kappaB p65 nuclear entry in T cells
-
these studies establish Slp-76 as a critical determinant of NK-cell development and NK cell mediated elimination of missing-self target cells in mice
-
Data show that a splice variant of SLP-76 signal transducing adaptor protein (SLP-76 or Lcp2) reduced the amount of SLP-76 protein by ~90%, disrupting immunogenic and tolerogenic pathways to different degrees.
-
this analysis identified 65 proteins not associated before with the Zap70-Lat-SLP-76 network and thus should provide cues for future functional experiments.
-
A yopH mutant survived better in the absence of neutrophils, indicating that neutrophil inactivation by YopH by targeting PRAM-1/SKAP-HOM and SLP-76/Vav/PLCgamma2 signaling hubs may be critical for Yersinia survival.
-
analysis of a costimulatory mechanism by which CXCL12 and antigen converge at SLP-76 microcluster formation to enhance T cell responses
-
Findings indicate that SLP-76 is an essential signaling component for basophil activation downstream of both FcepsilonRI and the IL-3 receptor.
-
These findings reveal a novel role for SLP-76 in CXCR4-mediated T lymphocyte trafficking.
-
a novel regulation mechanism of SLP-76 by ubiquitination and proteasomal degradation of activated SLP-76, which is mediated by Ser-376 phosphorylation, leading to down-regulation of TCR signaling.
-
Loss of SLP-76 has no effect on persistence of the antigen-specific CD4+ memory pool, suggesting that homeostatic turnover is not required for persistence of this population.
-
SLP-76 and ADAP are involved in E-selectin-mediated integrin activation and neutrophil recruitment to inflamed kidneys, which may underlie the development of life-threatening ischemia-reperfusion-induced acute kidney injury in humans.
-
Data show that development of the CD8+ ILLs present in SH2 domain-containing leukocyte protein, 76-kDa Y145F mice require Eomes and PLZF.
-
Loss of Lcp2 leads to loss of tonic T-cell receptor signals altering the rate of memory versus effector cell differentiation independent of initial T-cell expansion.
-
Loss of Lcp2 leads to loss of tonic T-cell receptor signals altering the generation but not the persistence of CD8+ memory T cells.
-
HPK1 competes with ADAP for SLP-76 binding and via Rap1 negatively affects T-cell adhesion.
-
While SLP-76 and LAT1 depend on each other for many of their functions, LAT2/SLP-76 interactions and SLP-76-independent LAT1 functions also mediate a positive signaling pathway downstream of FcepsilonRI in mast cells.
-
A nonhemostatic pathway in which platelet CLEC-2 receptors bind lymphatic endothelial PDPN and activate SLP-76 signaling to regulate embryonic vascular development.
