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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

SLC7A11 increases the amount of BAP1. 2 / 2

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"p53 binds to the SLC7A11 promoter, directly suppressing its transcription; the nuclear deubiquitinase (DUB) BAP1 represses SLC7A11 transcription by removing histone 2A ubiquitination from the SLC7A11 promoter; and KEAP1 represses SLC7A11 transcription through degrading NRF2, a master transcription factor of antioxidant response and regulator of SLC7A11."

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"A luciferase assay with the SLC7A11 promoter showed that overexpression of BAP1 WT, but not its C91A mutant, decreased luciferase activity, whereas BAP1 knockdown increased it, indicating that BAP1 regulates SLC7A11 transcription (XREF_SUPPLEMENTARY - XREF_SUPPLEMENTARY)."

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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...