Browse our anti-LAT (LAT) Antibodies

Human Linker For Activation of T Cells (LAT) interaction partners

1. LAT, once internalized, transits through the Golgi-trans-Golgi network (TGN), where it is repolarized to the immune synapse.

2. Discovery of a conserved proline-rich motif in LAT that mediates efficient LAT phosphorylation.

3. Plasma membrane LAT activation precedes vesicular recruitment defining two phases of early T-cell activation.

4. LAT1 overexpression represents a negative prognostic marker that has been linked to tumor grade, proliferating potential and angiogenesis and mediates intracellular transport of anticancer agents.

5. The dimerization-dependent, cooperative binding of the growth factor receptor-bound protein 2 family to LAT may increase antigen receptor sensitivity by reducing signalosome formation at incompletely phosphorylated linker of activated T cells LAT molecules, thereby prioritizing the formation of complete signalosomes.

6. Nur77 suppresses CD4(+) T cell proliferation and uncover a suppressive role for Irf4 in TH2 polarization; halving Irf4 gene-dosage leads to increases in GATA3(+) and IL-4(+) cells.

7. LAT and phospholipase C-gamma dephosphorylation by SHP-1 inhibits natural killer cell cytototoxicity

8. Study examined molecular mobility within LAT:Grb2:SOS assemblies on supported membranes by single-molecule tracking. Trajectory analysis reveals a discrete temporal transition to subdiffusive motion below a characteristic timescale, indicating that the LAT:Grb2:SOS assembly has the dynamical structure of a loosely entangled polymer.

9. Here we report that phosphotyrosine-mediated assembly of adaptor protein LAT networks yields two distinct kinetic species of the Ras activator SOS

10. Overexpression of LAT is associated with microcephaly.

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

12. this study shows that inherited LAT deficiency should be considered in patients with combined immunodeficiency with T-cell abnormalities

13. This is the first report of a LAT-related disease in humans, manifesting by a progressive combined immune deficiency with severe autoimmune disease.

14. Data show that LAT1 plays an important role in regulating the uptake of essential amino acids such as leucine into endometrial cancer cells. Increased ability of BCH compared to LAT1 shRNA at inhibiting Ishikawa spheroid area suggests that other LAT family members may also contribute to cell growth.

15. Data indicate that the T cell-specific adaptor protein (TSAd) SH2 domain interacts with CD6 antigen and linker for activation of T cells protein (LAT) phosphotyrosine (pTyr) peptides.

16. High expression of LAT1 and ASCT2 correlates with metastasis and invasion in esophageal squamous cell carcinoma.

17. IFT20 is required for the delivery of the intracellular pool of LAT to the immune synapse in naive primary T lymphocytes.

18. Data show that the palmitoylation mutation of linker for activation of T cells (LAT)attenuated the signal transduction induced by glycosylphosphatidylinositol-anchored CD59 antigen in T cells.

19. HSV-1-encoded Us3 protein interrupted TCR signaling and interleukin-2 production by inactivation of the linker for activation of T cells.

20. Patients with severe aplastic anemia had increased levels of LAT and disturbed Th1-Th2 balance.

Mouse (Murine) Linker For Activation of T Cells (LAT) interaction partners

1. LAT, once internalized, transits through the Golgi-trans-Golgi network (TGN), where it is repolarized to the immune synapse.

2. LatY136F knock-in mice displayed increased production of Th2-type IgG1 (a homologue of human IgG4) and developed multiple organ tissue lesions reminiscent of those seen in patients with of immunoglobulin G4-related disease (IgG4-RD). The development of these tissue lesions was highly sensitive to corticosteroid treatment like in IgG4-RD. LatY136F knock-in mouse strain represents a promising model for human IgG4-RD.

3. this study shows that the site-specific delivery of linker for activation of T cells (LAT) in asthmatic mouse model

4. IFT20 is required for the delivery of the intracellular pool of LAT to the immune synapse in naive primary T lymphocytes.

5. miR-155 regulates the delicate balance between PAK1-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.

6. provide evidence that CD28 and the TCR complex regulate NF-kappaB via different signaling modules of GRB-2/VAV1 and LAT/ADAP pathways respectively.

7. The result indicate that LAT-PLCg1 interaction is important for controlling IL-6 production by T cells and demonstrate a critical role of IL-6 in the development of the lymphoproliferative syndrome.

8. low level of LAT-PLC-gamma1 interaction was associated with Th2 polarized differentiation, and this may contribute to the etiology of asthma.

9. These results suggest that proteasome-mediated degradation is involved in hypophosphorylated LAT and PLCgamma1 in Dow2-induced anergic T cells. The novel CD3-specific Ab, Dow2, may provide us with a unique tool for inducing immunosuppression

10. Sos1 has distinct roles in acting as a scaffold to oligomerize the adaptor protein LAT, and in guanine nucleotide exchange activity

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

12. Data suggest that transmembrane adaptor protein LAT-PLCgamma1 (Phospholipase C gamma 1) signaling may function differently in various subsets of gammadelta T cells.

13. chemotaxis toward antigen is controlled in mast cells by a cross-talk among FcepsilonRI, tetraspanin CD9, transmembrane adaptor proteins NTAL and LAT, and cytoskeleton-regulatory proteins of the ERM family

14. LAT-mediated signaling is essential for the continuous expansion of CD8 T cells during T cell priming, but is not required for contraction and memory maintenance of CD8 T cells.

15. The lymphoproliferative disease observed in LAT-Y136F mutant mice is at least partially dependent on hyperactivation of Ras.

16. our data suggest that LAT acts as a positive regulator of RANKL-induced osteoclastogenesis.

17. LAT-deficient CTLs failed to upregulate FasL and produce gamma interferon after engagement with target cells and had impaired granule-mediated killing.

18. PECAM-1-mediated inhibition of GPVI-dependent platelet responses result from recruitment of SHP-2-p85 complexes to tyrosine-phosphorylated PECAM-1, which diminishes the association of PI3K with activatory signaling molecules Gab1 and LAT

19. Data implicate that LAT has positive and negative roles in the regulation of mature T cells.

20. 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.