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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

BAP1 activates ITPR3. 3 / 3

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"In the cytoplasm, BAP1 modulates the stability of the IP3R3 channel, which allows the flux of Ca + from the endoplasmic reticulum into the mitochondria, where Ca + is required for the Krebs cycle and, at higher doses, to execute apoptosis."

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"Thus , loss of BAP1 leads to decreased ITPR3 expression , decreased mitochondrial Ca2 + and reduced sensitivity of cancer cells to apoptosis ."

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"Loss of BAP1 therefore leads to loss of ITPR3 , which in turn reduces apoptotic mitochondrial calcium signals [ 6 ] ."

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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...