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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.

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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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USP26 activates SMAD7. 3 / 3

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"Conversely, knockdown of USP26 rapidly degrades SMAD7 resulting in TGF-beta receptor stabilization and enhanced levels of p-SMAD2."

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"In contrast, loss of USP26 rapidly degrades SMAD7 stabilizing the TGF-beta receptors leading to enhanced TGF-beta activity as observed by increased levels of phosphorylated SMAD2."

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"As loss of USP26 degrades SMAD7 leading to the stabilization of TbetaR, we evaluated the role of TbetaR and SMAD7 on clinical outcome."

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Statements

USP26 activates SMAD7. 3 / 3

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