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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

Kinase-active TGFBR2 activates SMAD3. 2 / 2

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bel

"\"Smad proteins mediate signaling by transforming growth factor-beta (TGF-beta) 1 superfamily members (1-3). Upon binding of TGF-beta to cell surface complexes of type I and type II receptor serine/threonine kinases, the type II receptor phosphorylates the type I receptor, which further phosphorylates the receptor-regulated (R-) Smads, Smad2 and Smad3 (3). Phosphorylated R-Smads oligomerize with the common mediator (Co) Smad4 and accumulate in the nucleus where they regulate gene expression.\""

16135802

➶

bel

"\"Smad proteins mediate signaling by transforming growth factor-beta (TGF-beta) 1 superfamily members (1-3). Upon binding of TGF-beta to cell surface complexes of type I and type II receptor serine/threonine kinases, the type II receptor phosphorylates the type I receptor, which further phosphorylates the receptor-regulated (R-) Smads, Smad2 and Smad3 (3). Phosphorylated R-Smads oligomerize with the common mediator (Co) Smad4 and accumulate in the nucleus where they regulate gene expression.\""

16135802

Our Sources:

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