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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

ATXN3 activates Cell Survival. 2 / 3

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"Altogether, these results further support our findings that ATX3 selectively fine‐tunes DSB repair by preventing extensive RNF8/K63‐ubiquitin signalling, which balances DSB repair pathway choice.Finally, if this model is correct, then removal of RNF8 in ATX3‐depleted cells should prevent excessive 5′‐DNA end resection and restore cell survival after IR."

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"Based on recent studies, we suggest that wildtype ATXN3 stabilizes, or regulates, proteins at various step of the DDR process to promote efficient repair and cell survival."

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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...