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143 results for “Btk”
Candidate compounds from the design of covalent Bruton's tyrosine kinase (BTK) inhibitors via focused deep generative modeling
<pre>A total of 1491 candidate inhibitors for covalent inhibition of BTK are deposited as SMILES strings together with 34 known covalent BTK inhibitors used to guide generative computational design. The study will be reported in a publication in Molecules under the authors' names.</pre>
Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 2
<p>The Tec-family kinase Btk contains a lipid-binding Pleckstrin homology and Tec homology (PH-TH) module connected by a proline-rich linker to a "Src module", an SH3-SH2-kinase unit also found in Src-family kinases and Abl. We showed previously that Btk is activated by PH-TH dimerization, which is triggered on membranes by the phosphatidyl inositol phosphate PIP<sub>3</sub>, or in solution by inositol hexakisphosphate (IP<sub>6</sub>) (Wang <em>et al.</em> 2015, https://doi.org/10.7554/eLife.06074). We now report that the ubiquitous adaptor protein growth-factor-receptor-bound protein 2 (Grb2) binds to and substantially increases the activity of PIP<sub>3</sub>-bound Btk on membranes. Using reconstitution on supported-lipid bilayers, we find that Grb2 can be recruited to membrane-bound Btk through interaction with the proline-rich linker in Btk. This interaction requires intact Grb2, containing both SH3 domains and the SH2 domain, but does not require that the SH2 domain be able to bind phosphorylated tyrosine residues – thus Grb2 bound to Btk is free to interact with scaffold proteins via the SH2 domain. We show that the Grb2-Btk interaction recruits Btk to scaffold-mediated signaling clusters in reconstituted membranes. Our findings indicate that PIP<sub>3</sub>-mediated dimerization of Btk does not fully activate Btk, and that Btk adopts an autoinhibited state at the membrane that is released by Grb2.</p>
Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 3
The Tec-family kinase Btk contains a lipid-binding Pleckstrin homology and Tec homology (PH-TH) module connected by a proline-rich linker to a "Src module", an SH3-SH2-kinase unit also found in Src-family kinases and Abl. We showed previously that Btk is activated by PH-TH dimerization, which is triggered on membranes by the phosphatidyl inositol phosphate PIP<sub>3</sub>, or in solution by inositol hexakisphosphate (IP<sub>6</sub>) (Wang <em>et al.</em> 2015, https://doi.org/10.7554/eLife.06074). We now report that the ubiquitous adaptor protein growth-factor-receptor-bound protein 2 (Grb2) binds to and substantially increases the activity of PIP<sub>3</sub>-bound Btk on membranes. Using reconstitution on supported-lipid bilayers, we find that Grb2 can be recruited to membrane-bound Btk through interaction with the proline-rich linker in Btk. This interaction requires intact Grb2, containing both SH3 domains and the SH2 domain, but does not require that the SH2 domain be able to bind phosphorylated tyrosine residues – thus Grb2 bound to Btk is free to interact with scaffold proteins via the SH2 domain. We show that the Grb2-Btk interaction recruits Btk to scaffold-mediated signaling clusters in reconstituted membranes. Our findings indicate that PIP<sub>3</sub>-mediated dimerization of Btk does not fully activate Btk, and that Btk adopts an autoinhibited state at the membrane that is released by Grb2.
Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 1
The Tec-family kinase Btk contains a lipid-binding Pleckstrin homology and Tec homology (PH-TH) module connected by a proline-rich linker to a "Src module", an SH3-SH2-kinase unit also found in Src-family kinases and Abl. We showed previously that Btk is activated by PH-TH dimerization, which is triggered on membranes by the phosphatidyl inositol phosphate PIP<sub>3</sub>, or in solution by inositol hexakisphosphate (IP<sub>6</sub>) (Wang <em>et al.</em> 2015, https://doi.org/10.7554/eLife.06074). We now report that the ubiquitous adaptor protein growth-factor-receptor-bound protein 2 (Grb2) binds to and substantially increases the activity of PIP<sub>3</sub>-bound Btk on membranes. Using reconstitution on supported-lipid bilayers, we find that Grb2 can be recruited to membrane-bound Btk through interaction with the proline-rich linker in Btk. This interaction requires intact Grb2, containing both SH3 domains and the SH2 domain, but does not require that the SH2 domain be able to bind phosphorylated tyrosine residues – thus Grb2 bound to Btk is free to interact with scaffold proteins via the SH2 domain. We show that the Grb2-Btk interaction recruits Btk to scaffold-mediated signaling clusters in reconstituted membranes. Our findings indicate that PIP<sub>3</sub>-mediated dimerization of Btk does not fully activate Btk, and that Btk adopts an autoinhibited state at the membrane that is released by Grb2.
Relapsing Forms of Multiple Sclerosis (RMS) Study of Bruton's Tyrosine Kinase (BTK) Inhibitor Tolebrutinib (SAR442168) (GEMINI 1)
ClinicalTrials.gov study NCT04410978. IPD Sharing: YES. Countries: 24. Publications: 1.
Nonrelapsing Secondary Progressive Multiple Sclerosis (NRSPMS) Study of Bruton's Tyrosine Kinase (BTK) Inhibitor Tolebrutinib (SAR442168) (HERCULES)
ClinicalTrials.gov study NCT04411641. IPD Sharing: YES. Countries: 31. Publications: 1.
Relapsing Forms of Multiple Sclerosis (RMS) Study of Bruton's Tyrosine Kinase (BTK) Inhibitor Tolebrutinib (SAR442168) (GEMINI 2)
ClinicalTrials.gov study NCT04410991. IPD Sharing: YES. Countries: 28. Publications: 1.
Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 1
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Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 2
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Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2: Part 3
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BTK Inhibitor BGB-3111 in Chinese Participants With Diffuse Large B-Cell Lymphoma (Non-GCB) and Indolent Lymphoma (FL and MZL)
ClinicalTrials.gov study NCT03520920. IPD Sharing: YES. Countries: 1. Publications: 0.
Study of BTK Inhibitor BGB-3111 in Chinese Subjects With Relapsed/Refractory Waldenström's Macroglobulinemia (WM)
ClinicalTrials.gov study NCT03332173. IPD Sharing: YES. Countries: 1. Publications: 2.
Study of BTK Inhibitor Zanubrutinib in Participants With Relapsed/Refractory Non-GCB Type Diffuse Large B Cell Lymphoma
ClinicalTrials.gov study NCT03145064. IPD Sharing: YES. Countries: 1. Publications: 0.
IN.PACT BTK Randomized Study to Assess Safety and Efficacy of IN.PACT 014 vs. PTA
ClinicalTrials.gov study NCT02963649. IPD Sharing: NO. Countries: 5. Publications: 1.
Open-label Phase 3 BTK Inhibitor Ibrutinib vs Chlorambucil Patients 65 Years or Older With Treatment-naive CLL or SLL
ClinicalTrials.gov study NCT01722487. IPD Sharing: NO. Countries: 16. Publications: 9.
Response to the SHINGRIX Varicella Zoster Virus (VZV) Vaccine in Chronic Lymphocytic Leukemia (CLL) and CLL Treated With Bruton's Tyrosine Kinase Inhibitor (BTK-I)
ClinicalTrials.gov study NCT03702231. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Pilot Study to Determine Effects of the Btk Inhibitor PCI-32765 on Leukemia Cell Kinetics and Trafficking, Using Heavy Water Labeling in Subjects With CLL and SLL
ClinicalTrials.gov study NCT01752426. IPD Sharing: Not stated. Countries: 1. Publications: 2.
ACP-196 (Acalabrutinib), a Novel Bruton Tyrosine Kinase (BTK) Inhibitor, for Treatment of Chronic Lymphocytic Leukemia, Richter's Syndrome or Prolymphocytic Leukemia
ClinicalTrials.gov study NCT02029443. IPD Sharing: YES. Countries: 3. Publications: 8.
Disrupt PAD BTK II Study With the Shockwave Peripheral IVL System
ClinicalTrials.gov study NCT05007925. IPD Sharing: Not stated. Countries: 2. Publications: 0.
LIFE-BTK Randomized Controlled Trial
ClinicalTrials.gov study NCT04227899. IPD Sharing: NO. Countries: 6. Publications: 2.
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