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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

AKT activates CYLD. 3 / 3

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"Because Akt is known as the major upstream regulator of GSK3beta XREF_BIBR XREF_BIBR, we investigated whether Akt mediates CYLD induced degradation of Smad3."

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"Additionally, YTHDC2 inactivated the protein kinase B (Akt) pathway by increasing CYLD in PTC cells."

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"CYLD deficiency-mediated Akt activation is instrumental for the apoptosis-resistant phenotypes of miR-130b."

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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...