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A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

This Project

INDRA is developed by indralabs, a part of the Harvard Medical School Laboratory of Systems Pharmacology.

This project, indra_db, is also developed by the indralab team. For more information on how we procure our sources, you can go here. This work was funded by ARO grant W911NF‐15‐1‐0544 under the DARPA Communicating with Computers program.

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Statements

TNFAIP3 inhibits MALT1. 2 / 2

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"Activation of NFkappabeta through the canonical pathway related to TCR activation requires MALT1 signaling, which is suppressed by TNFAIP3 through deubiquitination 37."

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"The fact that MALT-1 ubiquitination by TRAF6 is essential for TCR- and BCR-induced activation of NF-κB and evidence that MALT-1 plays an important role in the pathogenesis of several autoimmune diseases (e.g., Multiple Sclerosis; Brüstle et al., xref ; Mc Guire et al., xref ) and lymphomas (e.g., Marginal B zone lymphoma and ABC-DLBCL; Ngo et al., xref ; Vega et al., xref ) suggest that MALT-1 inhibition by A20 plays an important role in the prevention of autoimmunity and lymphomas (Figure xref )."

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INDRA allows us to combine the results from a multitude of sources. In particular, the INDRA Database draws on the following...