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This Service

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 Receptors, Antigen, B-Cell. 2 / 2

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"The fact that patients with N1 tumors benefitted exceptionally from ibrutinib suggests that the recurrent mutations in PRKCB, BCL10, IKBKB, TNFAIP3 and TNIP1 in these tumors might also potentiate chronic active BCR signaling and reinforce BTK dependency."

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"83 In ABC DLBCL, biallelic inactivation of TNFAIP3 (by mutations, deletions or both) occurs in 30% of cases and can coexist with mutations in both MYD88 and CD79B, suggesting that inactivation of TNFAIP3 can enhance both BCR and TLR signalling pathways."

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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...