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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.

IndraLab

Statements

TNFAIP3 activates NLRP3. 3 / 3

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"For example, Walle et al. showed that the negative regulation of NLRP3 inflammasome activation induced by A20 markedly protects against the onset of RA-associated inflammation and cartilage destruction, highlighting the contribution of the NLRP3 inflammasome to the pathology of RA [ xref ]."

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"Loss of TLR4 in endothelial cells increased TNFAIP3 levels, while decreasing NLRP3 pathway proteins."

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"Collectively, overexpressed TNFAIP3 could contribute to the progression of AP by activating RIP3/NLRP3 axis, providing a potential therapeutic target for AP treatment."

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Our Sources:

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