It is clear that HBsAg, as the HBV membrane protein, can activate the TLR signaling and thereby promote the release of inflammatory cytokines44.
Changes in the biochemical composition and hence the biophysical properties of cellular membrane domains can activate signal transduction and transcription pathways that modulate mitogenesis [3].
In a previous study, it was suggested that membrane tethering can activate Fu.
Although such a defense mechanism may prevent the toxin from directly killing the cell, the initial membrane disruption can activate immune pathways such as the NLRP3 inflammasome.
Once MUC1 becomes overexpressed and repositioned along the entire cell membrane, it can activate a number of receptor tyrosine kinases, most notably epidermal growth factor receptor (EGFR) [ 46].
Upon drought stress, changes in phospholipid composition are detected in plants and membrane phospholipids can activate groups of phospholipases that catalyze the formation of multiple second-messenger molecules [ 29].
Previous studies have shown that membrane depolarization can activate NMDARs in the synapse, which then in turn mediate the expression and phosphorylation state of CREB, and promote survival of neuronal cells.
This is consistent with data reported in β-thalassemia/HbE patients [ 27] and might be due to oxidation of protein band 3 on RBC membranes which can activate complement-mediated phagocytosis by macrophages, leading to phagocytosis of the damage RBC.
Moesin, a member of the FERM (4.1 protein, ezrin, radixin, moesin) domain-containing family of proteins interacting with cytosolic tails of trans-membrane proteins, can activate the IL-2/IL-2R pathway [ 48], a system well known to be inefficient in maintaining Treg cells in this model of autoimmunity.
