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ZAP70-expressing chronic lymphocytic leukemia cells show increased chemokine-driven arrest on immobilized integrin ligands and on chemokine-presenting endothelial cells under physiologic flow conditions
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this study shows that ZAP70 is a key signal transduction molecule in TCR signaling, and gene point mutations induced inflammatory arthritis in mice
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We have characterized the second mutation reported for the first SH2 domain of ZAP-70. Therefore, this study extends the genetic etiology and molecular characterization of ZAP-70 mutations that lead to early onset immunodeficiency.
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ZAP-70 was a strong prognostic biomarker for patients with CLL
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In this article, the authors have shown that Natural killer cells can reduce their functional role through downregulation of Syk and Zap70 kinases.
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These results identify a tight negative feedback loop in which ZAP-70-activated p38 reciprocally phosphorylates ZAP-70 and destabilizes the signaling complex.
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we have identified a new redox-active motif which is crucial for the regulation of Zap70 stability/activity. We believe that this motif has the potential to become a novel target for the development of therapeutic tools to modulate the expression/activity of kinases.
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The expression of COBLL1, LPL, and ZAP70 corresponded to patient prognosis and to IGHV mutational status, although not absolutely. When we combined all three markers together and performed the ROC analysis, AUC increased compared to the AUC of individual gene expression.
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The authors find that ZAP-70 selects its substrates by utilizing an electrostatic mechanism that excludes substrates with positively-charged residues and favors LAT and SLP-76 phosphosites that are surrounded by negatively-charged residues.
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The data describe the critical early step of directional cell movement toward SDF-1 that ZAP-70 is recruited to the CXCR4 at the leading edge of membrane and consequently modulates lamellipodia/filopodia formation and integrin activation.
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The study identified the criteria for the design of binders that specifically address either the Syk or the Zap-70 Tandem Src Homology 2 Domains, tSH2. While Syk tSH2 has a rather broad substrate scope, ZAP-70 tSH2 required a proximal arrangement of the phosphotyrosine ligands in defined strand orientation.
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ZAP-70 signaling was impaired by cholesterol depletion, further supporting the importance of membrane organization in TCR signaling.
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We conclude that ZAP70 plays a role for the homing to and/or the survival of ALL cells in the CNS and that ZAP70 may represent a therapeutic target. Furthermore, targeting CCR7/CXCR4 may be particularly promising in treating T-ALL.
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The aim of this study was to evaluate the expression of ZAP70 changing during disease progression, the intracellular interferon gamma (IFN-gamma) and IL-4 content of T and B lymphocytes and the CLL cell subset (CD5+CD19+) in CLL patients and healthy subjects, and ZAP70 correlation with cytokine production.
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in this study, authors discovered a cycle of recruitment, activation and release for Zap70 kinases at phosphorylated T-cell antigen receptors, which turned them into a 'catalytic unit' that amplified antigenic stimuli
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The histological observations suggested that the patients represent diverse cases of NHL like mature B-cell type, mature T-cell type and high grade diffuse B-cell type NHL. The findings indicate that patients with NHL may also be analyzed for status of PAX5, CD19 and ZAP70, and their transcriptional and post-translational variants for the differential diagnosis of NHL and therapy.
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Compound heterozygous mutations in ZAP70 gene is associated with leaky severe combined immunodeficiency disorder.
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The results suggest that genetic polymorphism in the 3' UTR of ZAP-70 is associated with rheumatoid arthritis susceptibility in southern Taiwanese.
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Cellular studies with ZAP70 showed that multiple lipids bind its C-terminal SH2 domain in a spatiotemporally specific manner and thereby exert exquisite spatiotemporal control over its protein binding and signaling activities in T cells.
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Whole-exome sequencing performed on five family members revealed two affected siblings to be compound heterozygous for two unique missense mutations in the 70-kD T cell receptor zeta-chain associated protein (ZAP-70).
