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anti-Mouse (Murine) ITK Antikörper:
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Human Monoclonal ITK Primary Antibody für ICC, FACS - ABIN969222
Huck, Feyen, Niehues, Rüschendorf, Hübner, Laws, Telieps, Knapp, Wacker, Meindl, Jumaa, Borkhardt: Girls homozygous for an IL-2-inducible T cell kinase mutation that leads to protein deficiency develop fatal EBV-associated lymphoproliferation. in The Journal of clinical investigation 2009
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Human Monoclonal ITK Primary Antibody für ELISA, WB - ABIN966422
Perez-Villar, ODay, Hewgill, Nadler, Kanner: Nuclear localization of the tyrosine kinase Itk and interaction of its SH3 domain with karyopherin alpha (Rch1alpha). in International immunology 2001
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Human Monoclonal ITK Primary Antibody für ELISA, WB - ABIN1724708
Graves, Siroux, Guerra, Klimecki, Martinez: Association of atopy and eczema with polymorphisms in T-cell immunoglobulin domain and mucin domain-IL-2-inducible T-cell kinase gene cluster in chromosome 5 q 33. in The Journal of allergy and clinical immunology 2005
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Human Monoclonal ITK Primary Antibody für FACS, ELISA - ABIN966423
Bradley, Griffin, Livingston: Relationship of oligomerization to enzymatic and DNA-binding properties of the SV40 large T antigen. in Cell 1982
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Human Polyclonal ITK Primary Antibody für ELISA, WB - ABIN256939
Tanaka, Asao, Ohtani, Nakamura, Sugamura: A novel human tyrosine kinase gene inducible in T cells by interleukin 2. in FEBS letters 1993
Our results provide new insight into the effect of ITK and suboptimal T-cell receptor signaling on CD8 (zeige CD8A Antikörper)(+) 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 Antikörper) regulate thermal homeostasis during septic response through mast cell function in mice.
Taken together, these data indicate that ITK plus RLK (zeige TXK Antikörper) inhibition may have therapeutic potential in Th1 (zeige HAND1 Antikörper)-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 Antikörper), Th2, and Th17 cells.
The kinase Itk and the adaptor TSAd (zeige SH2D2A Antikörper) change the specificity of the kinase Lck (zeige LCK Antikörper) in T cells by promoting the phosphorylation of Tyr192.
Data indicate that the interleukin-2 (zeige IL2 Antikörper) inducible tyrosine kinase (zeige TYRO3 Antikörper) K390R point mutation (Itk-KD) transgenic mice were largely protected from inflammatory symptoms in an Ovalbumin (zeige OVA Antikörper) model of airway inflammation.
The Itk pleckstrin (zeige PLEK Antikörper) homology domain binds to Calmodulin and PI(3,4,5)Pto promote efficient calcium signaling and IL-17A (zeige IL17A Antikörper) 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 Antikörper) genes, respectively.
These data indicate that PRN694 is a highly selective and potent covalent inhibitor of ITK and RLK (zeige TXK Antikörper), 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 Antikörper) in EGFR (zeige EGFR Antikörper)-dependent PC9 (zeige PCSK9 Antikörper) cells, and these genes include seven of nine Src (zeige SRC Antikörper) family kinase genes, FGFR1 (zeige FGFR1 Antikörper), FGFR2 (zeige FGFR2 Antikörper), ITK, NTRK1 (zeige NTRK1 Antikörper), NTRK2 (zeige NTRK2 Antikörper), MOS (zeige MOS Antikörper), MST1R (zeige MST1R Antikörper), and RAF1 (zeige RAF1 Antikörper).
ITK deficiency is a genetic cause of idiopathic CD4 (zeige CD4 Antikörper)+ 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