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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.

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Statements

PI3K_p85 binds IRS1 and PIK3CA. 2 / 2

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"Moreover, we observed that valsartan treatment exaggerated the insulin-induced phosphorylation of IRS-1, the association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3 kinase (PI 3-K), PI 3-K activity, and translocation of GLUT4 to the plasma membrane."

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"As expected, compared with normal chow-fed mice, insulin-induced AKT phosphorylation, tyrosine phosphorylation of IRS1 (insulin receptor substrate 1), and IRS1 interaction with p85-phosphoinositide 3 kinase (PI3K) were greatly reduced in adipose tissue, liver, and muscle of HFD-fed wild-type control mice ( xref ), demonstrating diet-induced insulin insensitivity of these tissues."

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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...