It has been proposed that coexpression of p75NTR and Trk receptors may induce receptors aggregation in lipid rafts, convergence of signaling pathways or recruitments of different intracellular adaptors [48], [49].
Our results showed that F3 may induce death receptor ligands to initiate signaling via receptor oligomerization, recruitment of specialized adaptor proteins and activation of caspase cascades.
Tang et al. [ 14] concluded that decreased dysbindin-1C in the dorsolateral prefrontal cortex may induce NMDA receptor hypofunction in fast-spiking interneurons contributing to the cognitive deficits of schizophrenia.
Our findings identify that NO seems to activate GRK, which may induce adrenergic receptors' desensitization to agonists, contributing to severe cardiovascular hyporesponsiveness observed during septic shock.
Our studies in vitro and in vivo analysis suggest that neuronal-specific EphB3 may induce dependence receptor-mediated cell death following the reduced expression or interaction with ephrinB3 in the adult CCI-injured forebrain that leads to reduced motor performance, a phenotype that is reversed upon administration of ephrinB3-Fc or in the absence of EphB3 (EphB3−/−).
In contrast, higher dose MPH may induce excessive catecholamine receptor stimulation throughout the brain and fail to ameliorate the performance on reversal and shifting set.
After autoantibody-binding to the respective myocardial antigen via the F ab 2 part and cross-linking via the Fc part to Fcγ receptors IIa, these receptors then may induce an activating signal via the FC receptor's cytoplasmic domain, thereby possibly triggering a cardiodepressive effect (see Figure 1I).
Our study showing synergism between LPA and troglitazone also suggests that different ligands activating a common nuclear receptor may induce different effects, including different sets of genes and biological activities [1].
Consequently, hypersensitivity of the 5-HT1 receptor may induce decreased production of 5-HT leading to higher dopamine levels [ 34].
Their findings suggest that IL-9 binging to its receptor may induce mucosal epithelial cell growth, epithelial cell proliferation, and inflammatory cell infiltration in CRS.
