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Our results provide new insight into the effect of ITK and suboptimal T-cell receptor signaling on CD8 (zeige CD8A Proteine)(+) 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 (zeige BTK Proteine) regulate thermal homeostasis during septic response through mast cell function in mice.
Taken together, these data indicate that ITK plus RLK (zeige TXK Proteine) inhibition may have therapeutic potential in Th1 (zeige HAND1 Proteine)-mediated inflammatory diseases.
This work has important implications for understanding the role of Itk signaling in the development versus function of iNKT cells, Th1 (zeige HAND1 Proteine), Th2, and Th17 cells.
The kinase Itk and the adaptor TSAd (zeige SH2D2A Proteine) change the specificity of the kinase Lck (zeige LCK Proteine) in T cells by promoting the phosphorylation of Tyr192.
Data indicate that the interleukin-2 (zeige IL2 Proteine) inducible tyrosine kinase (zeige TYRO3 Proteine) K390R point mutation (Itk-KD) transgenic mice were largely protected from inflammatory symptoms in an Ovalbumin (zeige OVA Proteine) model of airway inflammation.
The Itk pleckstrin (zeige PLEK Proteine) homology domain binds to Calmodulin and PI(3,4,5)Pto promote efficient calcium signaling and IL-17A (zeige IL17A Proteine) production.
Signaling by Itk promotes autoimmunity and CNS inflammation.
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 (zeige SYK Proteine) genes, respectively.
These data indicate that PRN694 is a highly selective and potent covalent inhibitor of ITK and RLK (zeige TXK Proteine), 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 (zeige EGFR Proteine) in EGFR (zeige EGFR Proteine)-dependent PC9 (zeige PCSK9 Proteine) cells, and these genes include seven of nine Src (zeige SRC Proteine) family kinase genes, FGFR1 (zeige FGFR1 Proteine), FGFR2 (zeige FGFR2 Proteine), ITK, NTRK1 (zeige NTRK1 Proteine), NTRK2 (zeige NTRK2 Proteine), MOS (zeige MOS Proteine), MST1R (zeige MST1R Proteine), and RAF1 (zeige RAF1 Proteine).
ITK deficiency is a genetic cause of idiopathic CD4 (zeige CD4 Proteine)+ T-cell lymphopenia.
Data indicate reduced T-cell activation by altered IL-2 inducible T-cell kinase (ITK) expression in vitro.
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