The protonated/deprotonated MUA ligand that caused changes in the dipole moment of molecules may trigger various degrees of electron pulling force (the carboxyl groups of MUA are electron-withdrawing groups[43]).
As listed in Table 1, a wide variety of xenobiotics and endogenous small molecules may trigger eryptosis.
The impaired cartilage properties that follow degradation of matrix molecules may trigger subsequent damage to the collagen network and attempts at matrix repair [ 13].
Having a list of these, we can perform an automated query in the Small Molecule Mechanisms Database to identify records of small molecules that may trigger the same pathway activity.
In turn, as shown in Figure 1C, this database can be queried, given a list of active signaling pathways derived from differential gene expression data, returning a set of small molecules that may trigger the same active pathways.
Molecules that may trigger engulfment by committed phagocytes have been identified to some extent (including phosphatidylserine, recognised by receptors such as CD36, CD68, or CD14), but much less is known about the molecular cascade that may occur with the 'amateur' or facultative phagocytes [ 15, 23].
It is most likely that DAMPs released from the necrotic cells and tissues resulting from their exposure to toxic molecules, such as ROS, may trigger inflammatory response.
Finally, using a list of active signaling pathways as query, a similarity search can identify small molecules from the database that may trigger these pathways.
LPS molecules, also known as bacterial endotoxins, may trigger acute and chronic inflammation, leading to immune cell activation and cytokine release.
Oligosaccharides may trigger conformational changes in the molecule and mask antigenic sites, which in turn would prevent binding of host antibodies.
