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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

CYLD increases the amount of RIPK1. 2 / 2

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"Furthermore, we demonstrate FMRP to be critically important for regulating key molecules in TNF receptor 1 (TNFR1)-dependent apoptosis and necroptosis including CYLD, c-FLIP S and JNK, which contribute to prolonged RIPK1 expression."

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"In contrast, overexpression of CYLD caused downregulation of RIPK1 in Mel-CV and ME1007 cells, which was nevertheless reversed by the treatment with the proteasome inhibitor MG132 (XREF_FIG), substantiating that downregulation of RIPK1 expression by CYLD is mediated by the proteasomal degradation XREF_BIBR."

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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...