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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

USP1 bound to WDR48 activates homologous recombination. 2 / 2

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"Additionally, the same study disrupted the NHEJ pathway, via knockout of Ku70 (also known as XRCC6 or X-Ray repair cross complementing 6), in UAF1 -/-/- cells which restored the cellular resistance to camptothecin and the PARP inhibitor suggesting that the USP1 and UAF1 complex promotes HR, at least in part by suppressing NHEJ."

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"A study in which USP1 -/-, UAF1 -/-/-, and USP1 -/- UAF1 -/-/- double-knockout DT40 cells showed hypersensitivity to camptothecin and an inhibitor of poly (ADP-ribose) polymerase (PARP), which suggests that the USP1 and UAF1 complex promotes HR."

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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...