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ITK signalling through the Ras/IRF4 pathway is required for functional development of type 1 regulatory T cells.
Data show that interleukin-2 inducible T cell kinase (Itk)negatively regulates the development of nTh1 cells that express interferon-gamma (IFNgamma) in a T-bet transcription factor (Tbet) independent manner.
Our results provide new insight into the effect of ITK and suboptimal T-cell receptor signaling on CD8(+) T cell function, and how these may contribute to phenotypes associated with ITK deficiency
Data suggest that the pleckstrin homology domain of Itk functions as a phospholipid bilayer recognition site that localizes Itk to membrane via phosphatidylinositol 3,4,5-trisphosphate (PIP3) binding; this specific binding inhibits the phospho-transfer reaction via an allosteric mechanism.
pharmacological inhibition of ITK resulted in T cell hyperplasia and the increased production of TH2-type cytokines.
ITK and BTK regulate thermal homeostasis during septic response through mast cell function in mice.
Taken together, these data indicate that ITK plus RLK inhibition may have therapeutic potential in Th1-mediated inflammatory diseases.
This work has important implications for understanding the role of Itk signaling in the development versus function of iNKT cells, Th1, Th2, and Th17 cells.
The kinase Itk and the adaptor TSAd change the specificity of the kinase Lck in T cells by promoting the phosphorylation of Tyr192.
Data indicate that the interleukin-2 inducible tyrosine kinase K390R point mutation (Itk-KD) transgenic mice were largely protected from inflammatory symptoms in an Ovalbumin model of airway inflammation.
The Itk pleckstrin homology domain binds to Calmodulin and PI(3,4,5)Pto promote efficient calcium signaling and IL-17A production.
Signaling by Itk promotes autoimmunity and CNS inflammation.
ITK thus regulates the development and function of Tregs.
Data indicate that the IL2-inducible T-cell kinase itk(-/-) innate zinc finger protein 145 PLZF(+)CD4(+) T cells express alphabeta TCRs, neither beta2-microglobulin-dependent MHC class I nor any MHC class II molecules are required for their development.
These findings suggest that some naive CD8(+) T cells may be preprogrammed by weak homeostatic TCR signals in the presence of IL-4 to become memory phenotype cells with the ability to elaborate effector function rapidly.
Data indicate reduced cardiac inflammation in with IL-2-inducible T-cell kinase (ITK) inhibition following Coxsackievirus B3 (CVB3) infection.
Data indicate that dendritic cells-MHCII and IL-2-inducible T cell kinase Itk regulate the development of innate memory phenotype (IMP) CD4(+) T cells, which suppresses the development of autoimmune disorder in syngeneic bone marrow transplantation.
Itk-mediated integration of T cell receptor and cytokine signaling regulates the balance between Th17 and regulatory T cells.
Data show that substitution of 6 of the 619 amino acid residues of Itk (interleukin-2-inducible T cell kinase) with the corresponding residues of Btk (Bruton's tyrosine kinase), and vice versa, completely switched the activities of Itk and Btk.
ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses.
These observations have significant therapeutic implications, as pharmacologic inhibition of ITK prevented the activation of this signaling axis and overcame chemotherapy resistance.
The data indicate that increased ITK expression could act as a disease activity marker and as a risk factor for involvement in SLE, but it still needs further study to confirm.
We conclude that ITK, formerly considered an immune cell-specific protein, is aberrantly expressed in melanoma and promotes tumor development and progression
Found that 38% and 14% of the Angioimmunoblastic T-cell lymphoma cases exhibited gains of ITK and SYK genes, respectively.
These data indicate that PRN694 is a highly selective and potent covalent inhibitor of ITK and RLK, and its extended target residence time enables durable attenuation of effector cells in vitro and in vivo.
approach identified 18 kinase and kinase-related genes whose overexpression can substitute for EGFR in EGFR-dependent PC9 cells, and these genes include seven of nine Src family kinase genes, FGFR1, FGFR2, ITK, NTRK1, NTRK2, MOS, MST1R, and RAF1.
ITK deficiency is a genetic cause of idiopathic CD4+ T-cell lymphopenia.
Data indicate reduced T-cell activation by altered IL-2 inducible T-cell kinase (ITK) expression in vitro.
T-cell-specific human ITK-Syk oncogene in mice leads to early polyclonal T cell lymphoproliferation with B cell expansion. It induces terminal T cell differentiation via Blimp-1, eliminating oncogene-expressing cells early in development.
Case Report/Letter: ITK/SYK translocation in angioimmunoblastic T-cell lymphoma.
a new pathway regulated by Itk in cells, and suggest cross talk between Itk and G-protein signaling downstream of the TcR.
Data indicate that the intracellular signaling of ITK-SYK requires both SLP-76 and the adapter function of SYK/ZAP-70 kinases.
ITK and Gag colocalized at the plasma membrane and were concentrated at sites of F-actin accumulation and membrane lipid rafts in HIV-1 infected T cells
DEF6, a novel substrate for the Tec kinase ITK, contains a glutamine-rich aggregation-prone region and forms cytoplasmic granules that co-localize with P-bodies.
This review focuses on Itk and its role in regulating T-cell signaling and function, especially the activation and development of alpha-beta T cells.
ITK mutations are distributed over the entire protein and include missense, nonsense and indel mutations, reminiscent of the situation in its sister kinase in B cells, Bruton's tyrosine kinase
These results indicate that Itk is required for efficient replication of influenza virus in infected T-cells.
This gene encodes an intracellular tyrosine kinase expressed in T-cells. The protein contains both SH2 and SH3 domains which are often found in intracellular kinases. It is thought to play a role in T-cell proliferation and differentiation.
, interleukin-2-inducible T cell kinase
, kinase TLK
, tyrosine-protein kinase ITK/TSK
, IL-2-inducible T cell kinase
, IL-2-inducible T-cell kinase
, homolog of mouse T-cell itk/tsk
, interleukin-2-inducible T-cell kinase
, kinase EMT
, tyrosine-protein kinase LYK