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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
this study shows that ZAP70 is a key signal transduction molecule in TCR signaling, and gene point mutations induced inflammatory arthritis in mice
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.
ZAP-70 was a strong prognostic biomarker for patients with CLL
In this article, the authors have shown that Natural killer cells can reduce their functional role through downregulation of Syk and Zap70 kinases.
These results identify a tight negative feedback loop in which ZAP-70-activated p38 reciprocally phosphorylates ZAP-70 and destabilizes the signaling complex.
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.
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.
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.
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.
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.
ZAP-70 signaling was impaired by cholesterol depletion, further supporting the importance of membrane organization in TCR signaling.
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.
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.
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
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.
Compound heterozygous mutations in ZAP70 gene is associated with leaky severe combined immunodeficiency disorder.
The results suggest that genetic polymorphism in the 3' UTR of ZAP-70 is associated with rheumatoid arthritis susceptibility in southern Taiwanese.
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.
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).
hypomorphic alleles of Zap70 or chemical inhibition of Zap70 catalysis leads to an increase of IFN-gamma-producing invariant natural killer T cells.
RanBP2 expression was regulated by Zap70.
disruption of normal Zap70 autoinhibition engaged negative feedback mechanisms by which negative selection and inhibitory receptors restrain TCR signaling to enforce both central and peripheral tolerance.
was significantly increased in 22-month AEW mice compared with 5-month AEW mice. ELISA data showed that secretions of IL-2 and NGF in 22-month AEW mice were higher than 5-month AEW mice. Our results indicate that increased ZAP70 is involved in dry skin in elderly pruritus. Increased secretion of IL-2 and NGF may induce dry skin itch.
this study shows that ZAP-70 mutation has a strong impact on T cell-driven arthritis in SKG model regardless of the genetic background
These findings establish Otud7b as a positive regulator of T cell receptor-proximal signaling and T cell activation, highlighting the importance of deubiquitination in regulating Zap70 function.
Data suggest that ring finger protein 41 Nrdp1 terminates T cell antigen receptors (TCRs) signaling by inactivating Zap70 kinase.
Zap70 as a structural protein regulates integrin-mediated control of actin and with its catalytic activity regulates T cell receptor-mediated control of actin and membrane remodelling during formation of the immunological synapse.
Blockade of CXCR7 suppressed MIF-mediated ERK- and zeta-chain-associated protein kinase (ZAP)-70 activation
mediates the CD4 lineage differentiation in response to Class II selecting ligands
In mice with spondylarthritis, microbiota content varied according to whether T cell receptor signal strength was normal or was impaired due to the ZAP-70(W163C) mutation.
expression of Zap70 protein was essential for both long-term survival of naive T cells and for their proliferation in response to lymphopenia.
ZAP-70 enhances the migration of malignant B-cells into the supportive microenvironment found in the bone marrow mainly by enhancing signaling and migration after CXCR4 stimulation.
Titration of Zap70 activity resulted in graded reductions in positive and negative selection but did not decrease the cumulative TCR signals integrated by positively selected OT-I cells
MIF promotes the migration of B cells through a ZAP-70-dependent pathway mediated by cooperative engagement of CXCR4 and CD74.
Report role of ZAP-70 kinase mutation/deletion on thymocyte-positive selection via CD69 signaling.
while the kinase domain of Syk is uniquely required for OC function that of Zap70 inhibits it.
The forced intrathymic administration of histocompatible hematopoietic stem cells can sustain long-term thymopoiesis in ZAP-70-immunodeficient mice.
ZAP70 recruitment to the TCR and ZAP70 activation, revealed by its phosphorylation at tyrosine residues 292 and 319, were inhibited in T cells with a mutation in the proline-rich sequence of CD3 epsilon.
The surface expression of CTLA-4 was increased in subclinical stages of paratuberculosis infection while levels of ZAP-70 were decreased in CD4+ T cells of both subclinical and clinical animals, indicating a change in T cell phenotype with disease state.
syk and zap-70 function redundantly in an early progenitor to promote the migration of intersegmental vessel angioblasts and lymphangioblasts that contribute to the thoracic duct, either downstream of, or in parallel to vegfa.
This gene encodes an enzyme belonging to the protein tyrosine kinase family, and it plays a role in T-cell development and lymphocyte activation. This enzyme, which is phosphorylated on tyrosine residues upon T-cell antigen receptor (TCR) stimulation, functions in the initial step of TCR-mediated signal transduction in combination with the Src family kinases, Lck and Fyn. This enzyme is also essential for thymocyte development. Mutations in this gene cause selective T-cell defect, a severe combined immunodeficiency disease characterized by a selective absence of CD8-positive T-cells. Two transcript variants that encode different isoforms have been found for this gene.
70 kDa zeta-associated protein
, 70 kDa zeta-chain associated protein
, syk-related tyrosine kinase
, tyrosine-protein kinase ZAP-70
, zeta-chain associated protein kinase, 70kD
, tyrosine-protein kinase zap-70
, syk-related protein tyrosine kinase
, zeta-chain (TCR) associated protein kinase 70kDa
, zeta-chain associated protein kinase 70kDa
, tyrosine-protein kinase ZAP-70-like