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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

TGFBR1 phosphorylates SMAD3 on S423. 2 / 2

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signor

"A major event leading to smad3 activation is the tgf-beta-induced, tbetari-mediated phosphorylation at two c-terminal serine residues, ser-423 and ser-425, which triggers dissociation of smad3 from its receptors to form a complex with smad4 and accumulate in the nucleus"

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reach

"Activated TbetaRI and JNK differentially phosphorylates the mediator Smad3 to become pSmad3C (Ser 423/425) and pSmad3L (Ser 213) and then transmits tumor-suppressive or oncogenic TGF-beta signaling, respectively, by mediating distinct transcriptional responses [XREF_BIBR, XREF_BIBR]."

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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...