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This Service

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

S100A9 bound to TLR4 activates ERK. 1 / 1

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"S100A9 binds TLR4 and thereby activates p38, Extracellular signalregulated kinase 1(ERK)1/2 and Jun N-terminal kinase signaling, and this TLR4associated S100A9 effect seems to be a part of the mechanism behind the adverse prognostic impact of S100A8.Taken together these studies suggest that TLR4 expression by AML cells is associated with an adverse prognosis (i.e., a part of a high-risk leukemic cell phenotype), and TLR4 inhibition can have a chemosensitizing and/or direct antileukemic effect."

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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...