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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

STAT1 activates mutated USP18. 1 / 1

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"This immunological response is explained by the impairment of STAT4 phosphorylation and IFN-γ production as the result of STAT1 hyperactivation.11 Another group of researchers attributed the susceptibility of Usp18lty9 mice to S. typhimurium or Mycobacterium tuberculosis infection to elevated levels of IL-10, IL-1β, or IL-17, in addition to the deregulation of autophagy markers.10 Surprisingly, the contradictory nature of these two results obtained with Usp18 knockout mice and Usp18lty9 mice can be explained by either the different backgrounds of the mice or the specific ENU-induced mutation of Usp18."

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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...