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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.

IndraLab

Statements

USP48 inhibits ICL. 2 / 2

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"Our data demonstrate that loss of USP48 does not restore FANCI and FANCD2 monoubiquitylation or FANCD2 recruitment at ICLs, but if USP48 targets one or more sites on H2A that can be recognized by these nucleases, then loss of USP48 might bypass the requirement of the FA proteins and allow the recruitment of FAN1 or SLX4 and subsequent unhooking of the ICL in an FA deficient background."

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"Re-introduction of exogenous wild-type USP48, but not the catalytically inactive C98S USP48 mutant, partially reduced ICL resistance of DeltaUSP48DeltaFANCC cells, thus indicating that lack of USP48 catalytic activity is important for the increased survival of DeltaUSP48DeltaFANCC cells."

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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...