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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.

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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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USP15 leads to the deubiquitination of TOP2A. 3 / 3

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"USP15 overexpression significantly reduced the endogenous ubiquitination of TOP2A, and silencing endogenous USP15 promoted TOP2A ubiquitination."

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"Accordingly, in the presence or absence of MG132, silencing endogenous USP15 promoted TOP2A ubiquitination (Figures 6I and 6J)."

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"The results revealed that USP15 significantly diminished TOP2A ubiquitination, suggesting that USP15 might be a potential TOP2A deubiquitinase (Figure 6B)."

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USP15 leads to the deubiquitination of TOP2A. 3 / 3

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