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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 JAK2 leads to the phosphorylation of STAT3 on Y705. 2 / 2

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"Maximal activation of STAT3 requires phosphorylation at both Tyr705 and Ser727 sites (14). Although JAK2 kinase is shown to be responsible for phosphorylating STAT3 at Tyr705, we have shown that IL-1 receptor associated kinase 1 (IRAK-1) is capable of selectively phosphorylating STAT3 at Ser727 (15)."

19380824

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"Induction of STAT3 Tyr705 and Ser727 phosphorylations by Galpha(s)QL was suppressed by inhibition of protein kinase A, Janus kinase 2/3, Rac1, c-Jun N-terminal kinase (JNK), or phosphatidylinositol 3-kinase, and a similar profile was observed in response to beta2-adrenergic receptor stimulation"

17008315

Our Sources:

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