Browse our anti-ITK (ITK) Antibodies

Mouse (Murine) IL2-Inducible T-Cell Kinase (ITK) interaction partners

1. Our results provide new insight into the effect of ITK and suboptimal T-cell receptor signaling on CD8 (show CD8A Antibodies)(+) T cell function, and how these may contribute to phenotypes associated with ITK deficiency

2. 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.

3. pharmacological inhibition of ITK resulted in T cell hyperplasia and the increased production of TH2-type cytokines.

4. ITK and BTK (show BTK Antibodies) regulate thermal homeostasis during septic response through mast cell function in mice.

5. Taken together, these data indicate that ITK plus RLK (show TXK Antibodies) inhibition may have therapeutic potential in Th1 (show HAND1 Antibodies)-mediated inflammatory diseases.

6. This work has important implications for understanding the role of Itk signaling in the development versus function of iNKT cells, Th1 (show HAND1 Antibodies), Th2, and Th17 cells.

7. The kinase Itk and the adaptor TSAd (show SH2D2A Antibodies) change the specificity of the kinase Lck (show LCK Antibodies) in T cells by promoting the phosphorylation of Tyr192.

8. Data indicate that the interleukin-2 (show IL2 Antibodies) inducible tyrosine kinase (show TYRO3 Antibodies) K390R point mutation (Itk-KD) transgenic mice were largely protected from inflammatory symptoms in an Ovalbumin (show OVA Antibodies) model of airway inflammation.

9. The Itk pleckstrin (show PLEK Antibodies) homology domain binds to Calmodulin and PI(3,4,5)Pto promote efficient calcium signaling and IL-17A (show IL17A Antibodies) production.

10. Signaling by Itk promotes autoimmunity and CNS inflammation.

Human IL2-Inducible T-Cell Kinase (ITK) interaction partners

1. These observations have significant therapeutic implications, as pharmacologic inhibition of ITK prevented the activation of this signaling axis and overcame chemotherapy resistance.

2. Our results provide new insight into the effect of ITK and suboptimal T-cell receptor signaling on CD8 (show CD8A Antibodies)(+) T cell function, and how these may contribute to phenotypes associated with ITK deficiency

3. 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.

4. We conclude that ITK, formerly considered an immune cell-specific protein, is aberrantly expressed in melanoma and promotes tumor development and progression

5. The kinase Itk and the adaptor TSAd (show SH2D2A Antibodies) change the specificity of the kinase Lck (show LCK Antibodies) in T cells by promoting the phosphorylation of Tyr192.

6. Found that 38% and 14% of the Angioimmunoblastic T-cell lymphoma cases exhibited gains of ITK and SYK (show SYK Antibodies) genes, respectively.

7. These data indicate that PRN694 is a highly selective and potent covalent inhibitor of ITK and RLK (show TXK Antibodies), and its extended target residence time enables durable attenuation of effector cells in vitro and in vivo.

8. approach identified 18 kinase and kinase-related genes whose overexpression can substitute for EGFR (show EGFR Antibodies) in EGFR (show EGFR Antibodies)-dependent PC9 (show PCSK9 Antibodies) cells, and these genes include seven of nine Src (show SRC Antibodies) family kinase genes, FGFR1 (show FGFR1 Antibodies), FGFR2 (show FGFR2 Antibodies), ITK, NTRK1 (show NTRK1 Antibodies), NTRK2 (show NTRK2 Antibodies), MOS (show MOS Antibodies), MST1R (show MST1R Antibodies), and RAF1 (show RAF1 Antibodies).

9. ITK deficiency is a genetic cause of idiopathic CD4 (show CD4 Antibodies)+ T-cell lymphopenia.

10. Data indicate reduced T-cell activation by altered IL-2 inducible T-cell kinase (ITK) expression in vitro.