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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

SCN5A inhibits FGF12. 2 / 2

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"A previous study14 reported that a variation in SCN5A (p.H1849R) could block the regulation of FGF12 and cause human arrhythmia."

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"The p.Q7R mutation reduced binding to the Na V 1.5 C-terminus and Na + channel current density, leading to Na + channel loss-of-function phenotype consistent with that in BrS.12, 13 Furthermore, Musa etal reported that a variation in SCN5A (p.H1849R) blocks the regulation of FGF12 and causes human arrhythmia.14 This evidence highlighted that the variations in FGF12 may affect the interaction between FGF12 and Na + channel, leading to arrhythmia."

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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...