Browse our anti-LCP2 (LCP2) Antibodies

Mouse (Murine) Lymphocyte Cytosolic Protein 2 (SH2 Domain Containing Leukocyte Protein of 76kDa) (LCP2) interaction partners

1. 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

2. slp-76 contributes to the regulation of the tissue distribution, PLZF, and cytokine expression of iNKT cells via ADAP-dependent and -independent mechanisms.

3. findings identify ACK1 as a novel SLP-76-associated protein-tyrosine kinase that modulates early activation events in T cells.

4. 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

5. 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

6. 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.

7. this analysis identified 65 proteins not associated before with the Zap70-Lat-SLP-76 network and thus should provide cues for future functional experiments.

8. 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.

9. analysis of a costimulatory mechanism by which CXCL12 and antigen converge at SLP-76 microcluster formation to enhance T cell responses

10. Findings indicate that SLP-76 is an essential signaling component for basophil activation downstream of both FcepsilonRI and the IL-3 receptor.

11. These findings reveal a novel role for SLP-76 in CXCR4-mediated T lymphocyte trafficking.

12. 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.

13. 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.

14. 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.

15. Data show that development of the CD8+ ILLs present in SH2 domain-containing leukocyte protein, 76-kDa Y145F mice require Eomes and PLZF.

16. 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.

17. Loss of Lcp2 leads to loss of tonic T-cell receptor signals altering the generation but not the persistence of CD8+ memory T cells.

18. HPK1 competes with ADAP for SLP-76 binding and via Rap1 negatively affects T-cell adhesion.

19. 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.

20. A nonhemostatic pathway in which platelet CLEC-2 receptors bind lymphatic endothelial PDPN and activate SLP-76 signaling to regulate embryonic vascular development.

Human Lymphocyte Cytosolic Protein 2 (SH2 Domain Containing Leukocyte Protein of 76kDa) (LCP2) interaction partners

1. a previously unappreciated role for PLC-gamma1 in the positive regulation of Zap-70 and T-cell receptor tyrosine phosphorylation. Conversely, PLC-gamma1 negatively regulated the phosphorylation of SLP-76-associated proteins, including previously established Lck substrate phosphorylation sites within this complex.

2. These data are consistent with a model in which bivalent recruitment of a GADS/SLP-76 complex is required for costimulation by CD6.

3. LAT and SLP-76 are randomly dispersed throughout the clusters that form upon T cell receptor engagement.

4. SLP76 is ectopically expressed in chronic lymphocytic leukemia cells where it plays a role in B-cell receptor signaling.

5. findings identify ACK1 as a novel SLP-76-associated protein-tyrosine kinase that modulates early activation events in T cells.

6. Data strongly suggest that chemokine-stimulated associations between Vav1, SLP-76, and ADAP facilitate Rac1 activation and alpha4beta1-mediated adhesion, whereas Pyk2 opposes this adhesion by limiting Rac1 activation.

7. TSAD binds to and co-localizes with Nck. Expression of TSAD increases both Nck-Lck and Nck-SLP-76 interaction in T cells.

8. 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

9. SLP-76 N-terminal tyrosine residues regulate a dynamic signaling equilibrium involving feedback of proximal T-cell receptor signaling

10. analysis of a costimulatory mechanism by which CXCL12 and antigen converge at SLP-76 microcluster formation to enhance T cell responses

11. Multipoint binding of SLP-76 to ADAP facilitates the assembly of SLP-76 microclusters.

12. Data indicate a role for the SAM domain in mediating SLP-76 self-association for T-cell function.

13. Data indicate that the intracellular signaling of ITK-SYK requires both SLP-76 and the adapter function of SYK/ZAP-70 kinases.

14. Unique modes of regulation of positive and negative feedback pathways in T cells by SLP-76.

15. These findings reveal a novel role for SLP-76 in CXCR4-mediated T lymphocyte trafficking.

16. 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.

17. Complementary phosphorylation sites in the adaptor protein SLP-76 promote synergistic activation of natural killer cells.

18. Nef employs a dual mechanism to disturb early TCR signaling by limiting the communication between LAT and SLP-76

19. both T cell activation and the association between SLP-76 and Nck. After T cell receptor stimulation, SLP-76 was phosphorylated, which enabled the binding of Nck.

20. our studies demonstrate a novel role for the adaptor molecule SLP-76 in regulating HIV-1 infection in T cells