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Human Bruton Agammaglobulinemia tyrosine Kinase (BTK) interaction partners

1. Ibrutinib-resistant TMD8 cells had higher BCL2 (show BCL2 Antibodies) gene expression and increased sensitivity to ABT-199, a BCL-2 (show BCL2 Antibodies) inhibitor. Consistently, clinical samples from ABC (show ABCB6 Antibodies)-DLBCL patients who experienced poorer response to ibrutinib had higher BCL2 (show BCL2 Antibodies) gene expression. We further demonstrated synergistic growth suppression by ibrutinib and ABT-199 in multiple ABC (show ABCB6 Antibodies)-DLBCL, GCB (show GBA Antibodies)-DLBCL, and follicular lymphoma cell lines.

2. BTK-mediated signaling was found to be highly attenuated accompanied by a shift in PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) and apoptosis regulation-associated genes/proteins. Cytotoxicity studies using the AKT (show AKT1 Antibodies) inhibitor, MK2206+/-ibrutinib, and the Bcl-2 (show BCL2 Antibodies)-specific inhibitor, venetoclax+/-ibrutinib, demonstrated synergistic loss of cell viability

3. BTK-inhibitor ibrutinib and FK866 resulted in a significant and synergistic anti-Waldenstrom macroglobulinemia cell death, regardless of MYD88 (show MYD88 Antibodies) and CXCR4 (show CXCR4 Antibodies) mutational status.

4. Strong synergism was observed with pimasertib combined with the PI3K (show PIK3CA Antibodies) 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.

5. these data show that BTK is a critical NLRP3 (show NLRP3 Antibodies) inflammasome regulator

6. Resistant BTK mutants reconstituted B cell receptor-triggered chemokine (show CCL1 Antibodies) 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.

7. Bone marrow mesenchymal stem cells could increase myeloma stemness via activation of the BTK signal pathway.

8. 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.

9. this study elucidated mechanisms of BCL2 (show BCL2 Antibodies) overexpression and association of this survival pathway with the BCR (show BCR Antibodies)/BTK signaling pathway in MCL (show FH Antibodies), and revealed the role of BTK in noncanonical NF-kappaB (show NFKB1 Antibodies) activation, which also promotes cancer cell survival.

10. BTK, via p65BTK expression, is a novel and powerful oncogene (show RAB1A Antibodies) acting downstream of the RAS/MAPK (show MAPK1 Antibodies) pathway and suggest that its targeting may be a promising therapeutic approach.

Mouse (Murine) Bruton Agammaglobulinemia tyrosine Kinase (BTK) interaction partners

1. 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 Antibodies) 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.

2. acalabrutinib showed increased BTK selectivity compared with ibrutinib while demonstrating significant antitumor efficacy in vivo on par (show AFG3L2 Antibodies) with ibrutinib. Similarly, in the TCL1 (show TCL1A Antibodies) adoptive transfer model, decreased phosphorylation of BTK, PLCgamma2 (show PLCG2 Antibodies), and S6 was observed. Most notably, treatment with acalabrutinib resulted in a significant increase in survival compared with mice receiving vehicle

3. these data show that BTK is a critical NLRP3 (show NLRP3 Antibodies) inflammasome regulator

4. Rictor (show RICTOR Antibodies) positively regulates B cell receptor signaling via up-regulating Btk and down-regulating SH2-containing inositol phosphatase (show INPP5D Antibodies)

5. The pre-B-cell receptor (pre-BCR (show BCR Antibodies)) signaling molecules BLNK (show BLNK Antibodies), BTK and BANK1 (show BANK1 Antibodies) were positively regulated by the ZFP521 (show ZNF521 Antibodies) gene, leading to enhancement of the pre-BCR (show BCR Antibodies) signaling pathway.

6. these data indicate that in mature B cells, Tec (show NR4A3 Antibodies) and Btk may compete for activation of the Akt (show AKT1 Antibodies) signaling pathway, whereby the activating capacity of Btk is limited by the presence of Tec (show NR4A3 Antibodies) kinase.

7. 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

8. Inhibition of Btk by inhalation of aerosolized RN983 may be effective as a stand-alone asthma therapy.

9. Btk and NLRP3 (show NLRP3 Antibodies) co-regulate platelet activation, aggregation, and in vitro thrombus formation.The NLRP3 (show NLRP3 Antibodies) inflammasome is upregulated in activated platelets.

10. Btk inhibition ameliorated hepatocellular injury in a well-established model of liver partial warm ischemia and in situ reperfusion.

Cow (Bovine) Bruton Agammaglobulinemia tyrosine Kinase (BTK) interaction partners

1. inositol hexakisphosphate (IP6 (show GPRIN2 Antibodies)), a soluble signaling molecule found in both animal and plant cells, also activates Btk.