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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

TGFBR2 increases the amount of SMAD2. 1 / 1

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"Noteworthy, the SP cells sustain Bmpr1a (Alk3) and Bmpr2 (BMPRII) expression, and upregulate Alk5 (Tgfbr1) and TbetaRII (Tgfbr2), which lead to increased levels of pSmad2."

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Kinase-active TGFBR2 increases the amount of SMAD2 bound to SMAD3 and SMAD4. 1 / 1

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"a dimeric Smac/DIABLO molecule is required for binding to BIR2, but not to BIR3, which indicates significant differences in the affinity or mechanism by which Smac/DIABLO binds to these domains Figure 5: Association of IAPs with signalling complexes."

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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...