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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.
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
was significantly increased in 22-month AEW mice compared with 5-month AEW mice. ELISA data showed that secretions of IL-2 (show IL2 Proteins) and NGF (show NGFB Proteins) 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 (show IL2 Proteins) and NGF (show NGFB Proteins) 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 (show OTUD7B Proteins) 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 (show RNF41 Proteins) 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 (show CXCR7 Proteins) suppressed MIF (show MIF Proteins)-mediated ERK (show EPHB2 Proteins)- and zeta-chain-associated protein kinase (show CDK7 Proteins) (ZAP)-70 activation
mediates the CD4 (show CD4 Proteins) 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.
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 (show ORC3 Proteins) and SLP-76 (show LCP2 Proteins) phosphosites that are surrounded by negatively-charged residues.
The data describe the critical early step of directional cell movement toward SDF-1 (show CXCL12 Proteins) that ZAP-70 is recruited to the CXCR4 (show CXCR4 Proteins) 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 (show SYK Proteins) or the Zap-70 Tandem Src (show SRC Proteins) Homology 2 Domains, tSH2. While Syk (show SYK Proteins) 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 (show CCR7 Proteins)/CXCR4 (show CXCR4 Proteins) 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 (show IFNG Proteins)) and IL-4 (show IL4 Proteins) content of T and B lymphocytes and the CLL cell subset (CD5 (show CD5 Proteins)+CD19 (show CD19 Proteins)+) in CLL patients and healthy subjects, and ZAP70 correlation with cytokine production.
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 (show PRKDC Proteins) disorder.
The surface expression of CTLA-4 (show CTLA4 Proteins) was increased in subclinical stages of paratuberculosis infection while levels of ZAP-70 were decreased in CD4 (show CD4 Proteins)+ T cells of both subclinical and clinical animals, indicating a change in T cell phenotype with disease state.
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.
zeta-chain (TCR) associated protein kinase 70kDa
, zeta-chain associated protein kinase 70kDa
, tyrosine-protein kinase zap-70
, tyrosine-protein kinase ZAP-70-like
, 70 kDa zeta-associated protein
, 70 kDa zeta-chain associated protein
, syk-related tyrosine kinase
, tyrosine-protein kinase ZAP-70
, syk-related protein tyrosine kinase
, zeta-chain associated protein kinase, 70kD