Analysis of the Effects of the Bruton's tyrosine kinase (Btk) Inhibitor Ibrutinib on Monocyte Fcγ Receptor (FcγR) Function
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Title
Analysis of the Effects of the Bruton's tyrosine kinase (Btk) Inhibitor Ibrutinib on Monocyte Fcγ Receptor (FcγR) Function
Authors
Keywords
-
Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 291, Issue 6, Pages 3043-3052
Publisher
American Society for Biochemistry & Molecular Biology (ASBMB)
Online
2015-12-02
DOI
10.1074/jbc.m115.687251
References
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- Ibrutinib interferes with the cell-mediated anti-tumor activities of therapeutic CD20 antibodies: implications for combination therapy
- (2014) F. D. Roit et al. HAEMATOLOGICA
- Dual Functions of Bruton's Tyrosine Kinase and Tec Kinase during Fc Receptor-Induced Signaling and Phagocytosis
- (2014) J. Jongstra-Bilen et al. JOURNAL OF IMMUNOLOGY
- Safety and activity of ibrutinib plus rituximab for patients with high-risk chronic lymphocytic leukaemia: a single-arm, phase 2 study
- (2014) Jan A Burger et al. LANCET ONCOLOGY
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- Fc receptor-targeted therapies for the treatment of inflammation, cancer and beyond
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- Bruton tyrosine kinase represents a promising therapeutic target for treatment of chronic lymphocytic leukemia and is effectively targeted by PCI-32765
- (2011) S. E. M. Herman et al. BLOOD
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- (2011) Payal Mehta et al. PLoS One
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- (2011) Betty Y Chang et al. ARTHRITIS RESEARCH & THERAPY
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- (2010) L. A. Honigberg et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
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- Colocalization of the IL-12 receptor and Fc RIIIa to natural killer cell lipid rafts leads to activation of ERK and enhanced production of interferon-
- (2008) S. V. Kondadasula et al. BLOOD
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