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Study shows that high BTK expression predicts poor outcome in patients with glioma. Its overexpression is required for EGFR (show EGFR Proteins)-induced NF-kappaB (show NFKB1 Proteins) activation.
The Btk-dependent PIP5K1gamma lipid kinase activation by Fas (show FAS Proteins) counteracts FasL (show FASL Proteins)-induced cell death.
Ibrutinib-resistant TMD8 cells had higher BCL2 (show BCL2 Proteins) gene expression and increased sensitivity to ABT-199, a BCL-2 (show BCL2 Proteins) inhibitor. Consistently, clinical samples from ABC (show ABCB6 Proteins)-DLBCL patients who experienced poorer response to ibrutinib had higher BCL2 (show BCL2 Proteins) gene expression. We further demonstrated synergistic growth suppression by ibrutinib and ABT-199 in multiple ABC (show ABCB6 Proteins)-DLBCL, GCB (show GBA Proteins)-DLBCL, and follicular lymphoma cell lines.
BTK-mediated signaling was found to be highly attenuated accompanied by a shift in PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) and apoptosis regulation-associated genes/proteins. Cytotoxicity studies using the AKT (show AKT1 Proteins) inhibitor, MK2206+/-ibrutinib, and the Bcl-2 (show BCL2 Proteins)-specific inhibitor, venetoclax+/-ibrutinib, demonstrated synergistic loss of cell viability
BTK-inhibitor ibrutinib and FK866 resulted in a significant and synergistic anti-Waldenstrom macroglobulinemia cell death, regardless of MYD88 (show MYD88 Proteins) and CXCR4 (show CXCR4 Proteins) mutational status.
Strong synergism was observed with pimasertib combined with the PI3K (show PIK3CA Proteins) inhibitor idelalisib and the BTK inhibitor ibrutinib in cell lines derived from diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma. The data were confirmed in an in vivo experiment treating DLBCL xenografts with pimasertib and ibrutinib.
these data show that BTK is a critical NLRP3 (show NLRP3 Proteins) inflammasome regulator
Resistant BTK mutants reconstituted B cell receptor-triggered chemokine (show CCL1 Proteins) secretion in the presence of corresponding inhibitors, demonstrating that BTK activity is connected with cell-intrinsic functions of malignant B cells with importance for their dialogue with the micro-environment.
Bone marrow mesenchymal stem cells could increase myeloma stemness via activation of the BTK signal pathway.
the results show that the interaction between BTK and ANKRD54 is highly selective, since it was also identified in a screen using human SH3-domainome. A novel finding is that BTK not only binds to ANKRD54, but stands out as the preferred interactor, being highly dominant over all other human SH3-domains.
As chronic lymphocytic leukemia (CLL) proliferation and survival depends on the microenvironment, we used murine models to assess the efficacy of the BTK inhibitor acalabrutinib combined with the PI3Kdelta inhibitor ACP-319 in vivo.The combination of acalabrutinib and ACP-319 was superior to single-agent treatment in a murine CLL model
Results show that BTK adopts a closed conformation in dynamic equilibrium with open, active conformations. BTK lacks the phosphotyrosine regulatory tail of the SRC (show SRC Proteins) kinases, yet nevertheless achieves a phosphotyrosine-independent C-terminal latch. The unique proline-rich region is an internal "on" switch pushing the autoinhibited kinase toward its active state.
acalabrutinib showed increased BTK selectivity compared with ibrutinib while demonstrating significant antitumor efficacy in vivo on par (show AFG3L2 Proteins) with ibrutinib. Similarly, in the TCL1 (show TCL1A Proteins) adoptive transfer model, decreased phosphorylation of BTK, PLCgamma2 (show PLCG2 Proteins), and S6 was observed. Most notably, treatment with acalabrutinib resulted in a significant increase in survival compared with mice receiving vehicle
Rictor positively regulates B cell receptor signaling via up-regulating Btk and down-regulating SH2-containing inositol phosphatase (show INPP5D Proteins)
The pre-B-cell receptor (pre-BCR (show BCR Proteins)) signaling molecules BLNK (show BLNK Proteins), BTK and BANK1 (show BANK1 Proteins) were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR (show BCR Proteins) signaling pathway.
these data indicate that in mature B cells, Tec (show NR4A3 Proteins) and Btk may compete for activation of the Akt (show AKT1 Proteins) signaling pathway, whereby the activating capacity of Btk is limited by the presence of Tec (show NR4A3 Proteins) kinase.
these data demonstrate that enhanced BTK signaling in B cells can establish a T cell-driven proinflammatory loop resulting in autoimmune pathology, making BTK inhibition an attractive therapeutic strategy
Inhibition of Btk by inhalation of aerosolized RN983 may be effective as a stand-alone asthma therapy.
Btk and NLRP3 (show NLRP3 Proteins) co-regulate platelet activation, aggregation, and in vitro thrombus formation.The NLRP3 (show NLRP3 Proteins) inflammasome is upregulated in activated platelets.
inositol hexakisphosphate (IP6 (show GPRIN2 Proteins)), a soluble signaling molecule found in both animal and plant cells, also activates Btk.
The protein encoded by this gene plays a crucial role in B-cell development. Mutations in this gene cause X-linked agammaglobulinemia type 1, which is an immunodeficiency characterized by the failure to produce mature B lymphocytes, and associated with a failure of Ig heavy chain rearrangement.
Bruton agammaglobulinemia tyrosine kinase
, B-cell progenitor kinase
, agammaglobulinaemia tyrosine kinase
, dominant-negative kinase-deficient Brutons tyrosine kinase
, tyrosine-protein kinase BTK
, tyrosine-protein kinase BTK isoform (lacking exon 14)
, Bruton's tyrosine kinase
, Tyrosine-protein kinase BTK (Brutons tyrosine kinase) (Agammaglobulinaemia tyrosine kinase) (ATK) (B cell progenitor kinase) (BPK) (Kinase EMB)
, X-linked immune deficiency
, agammaglobulinemia tyrosine kinase
, bruton tyrosine kinase
, kinase EMB