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We postulate that numerous factors change receptor expression, signaling pathways, and secretion efficiency of MCs and that a combination of multiple, sometimes subtle phenotypic modifications can determine the response of a MC in a given time and place with the resulting homeostatic or pathophysiological responses (Figure 1)

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Noteworthy, intermolecular disulfide cross-links and glutathionylation enhance mutant SOD1 aggregation (Cozzolino et al., 2011