Abstract
A key feature of aggressive B cell lymphomas is constitutive NF-kappaB activation, which requires signals from the CARD11-BCL-10-MALT1 (CMB) complex. The unique enzymatic activity of MALT1 degrades one of its binding partners, BCL-10, as well as the NF-kappaB inhibitor A20. New data shows that targeting MALT1 protease activity may be a promising therapeutic strategy for treating aggressive B cell lymphomas.
MeSH terms
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Animals
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Caspase Inhibitors
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Caspases / chemistry
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Caspases / metabolism*
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Cell Proliferation / drug effects
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Cell Survival / drug effects
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Cytotoxicity, Immunologic / drug effects
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Humans
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Lymphoma, B-Cell / enzymology*
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Lymphoma, B-Cell / immunology
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Lymphoma, B-Cell / pathology
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Lymphoma, B-Cell / therapy*
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Protease Inhibitors / pharmacology
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Signal Transduction / drug effects
Substances
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Caspase Inhibitors
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Protease Inhibitors
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Caspases