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MALT1 inhibits CYLD. 15 / 16
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"Human paracaspase MALT1 is central to plasticity of lymphocytes as MALT1 proteolytic inactivation of CYLD ensures sustained activation of NFkappaB as well as RIG1 for providing innate immune response [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"MALT1 proteolytically cleaves and inactivates A20 as well as CYLD, two negative regulators of NF-κB signaling ( xref , xref )."
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"MALT-1 has been shown to inactivate A20, which in turn can lead to the activation of NF-κB (Coornaert et al., 2008), and can also inactivate CYLD (Staal et al., 2011)."
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"MALT1-dependent cleavage suppresses activity of CYLD and promotes its proteosomal degradation."
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"In summary, our study demonstrates for the first time that (i) MALT1 modulates TLR7 agonist- and IAV induced MMP-9 response in alveolar macrophages; (ii) MALT1 mediates CYLD reduction in macrophages upon TLR7 stimulation; (iii) MMP-9 production in alveolar macrophages is through NF-kappaB but not AP-1; and that (iv) MALT1 deficiency results in reduced IAV induced disease severity."
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"Here, we demonstrate that low expression of CYLD is associated with a poor prognosis of (ABC) DLBCL and MCL patients, and that chronic BCR signaling controls cleavage-mediated inactivation of CYLD by the paracaspase MALT1, followed by rapid proteasomal degradation."
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"In addition, our findings suggest that inhibition of MALT1-mediated CYLD cleavage, through other BCR signalosome inhibitors such as ibrutinib and sotrastaurin, contributes to the anti-tumor effects of these drugs."
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"Here, we show that T-cell receptors (TCR) activation, as well as overexpression of the oncogenic API2-MALT1 fusion protein, results in proteolytic inactivation of CYLD by MALT1, which is specifically required for c-jun N-terminal kinase (JNK) activation and the inducible expression of a subset of genes."
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"Here, we show that T-cell receptors (TCR) activation, as well as overexpression of the oncogenic API2-MALT1 fusion protein, results in proteolytic inactivation of CYLD by MALT1, which is specifically required for c-jun N-terminal kinase (JNK) activation and the inducible expression of a subset of genes."
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"CYLD but Not RelB Nor Regnase-1 Is Reduced by MALT1 Activity in Macrophages."
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"Because A20 and CYLD are deubiquitinases targeting K63-type polyubiquitin chains and are responsible for suppressing NF-κB activation, inactivation of A20 and CYLD by Malt1 is expected to potentiate N[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Inhibition of MALT1 activity by z-VRPR-fmk reversed CYLD degradation slightly but the difference did not reach statistical significance."
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"MALT1 paracaspase protease activity synergizes with TRAF6 by cleaving inhibitory molecules (e.g., A20, CYLD) and modulates other cellular functions by cleaving other substrates ."
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"Human paracaspase MALT1 is central to plasticity of lymphocytes as MALT1 proteolytic inactivation of CYLD ensures sustained activation of NFκB as well as RIG1 for providing innate immune response ( Be[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
25500259
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"T-cell receptor induced JNK activation requires proteolytic inactivation of CYLD by MALT1."
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