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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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USP9X activates homologous recombination. 4 / 4

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"HR assays showed that knockdown of USP9X significantly reduced HR efficiency, which was partially rescued by reintroduction of BRCA1 into USP9X-depleted cells."

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"Therefore, if USP9x increases MCL-1 expression [XREF_BIBR], then it could be suggested the USP9x indirectly promotes HR repair via MCL-1."

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"Together, these data suggest that USP9X promotes HR repair of DSB partially through BRCA1.3.5 USP9X depletion increases the sensitivity of cancer cells to DNA-damaging agents."

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"Together, these results suggest that USP9X interacts with BRCA1.3.4 USP9X promotes HR repair partially through BRCA1."

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Statements

USP9X activates homologous recombination. 4 / 4

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