Our data suggest that HER2 activity, which is suppressed in resistance involving L but not T alone, dictates whether β1 mediates an alternative pathway driving resistance.
At present, we do not understand the mechanism of constitutive c-MET phosphorylation in this cell line, but it is conceivable that signaling is mediated through an alternative co-receptor or as yet unidentified c-MET activating mutations.
Because Sorafenib completely blocks IGF-I activation of the RAF-MEK-ERK pathway (Figure 3), these results suggest that the rescue of the neuroblast population by IGF-I is mediated by an alternative pathway.
Nevertheless, we revealed that the activation of Nrf2 by HBx is mediated by an alternative more direct way.
However, this scenario is not consistent with the argument that the ethylene receptor signaling can be mediated to an alternative pathway that is independent of CTR1.
Critically the extent to which their clinical activity is dependent on re-induction of epigenetically silenced tumour suppressor or pro-apoptotic genes or whether their anti-tumor effect is mediated through an alternative mechanism remains unknown.
Potential explanations for these results might be that first, TEA-sensitive K+ channels are absent from PC axons and/or their NoRs and repolarization is mediated by an alternative mechanism.
Although counterintuitive, this finding is in line with previous results in 5-LOX−/− mice [ 1] and may be mediated by an alternative cyclooxygenase-dependent pathway in the absence of LOX [ 13].
We therefore propose that PMT-induced miR-21 upregulation is mediated by an alternative pathway of miR-21 induction [ 40– 43] that involves the signal transducer and activator of transcription (STAT -3, a well-known downSTAT -3target of PMT signalling [ 44] (Additional file 2: Figure S2B).
Indeed, this supposition is supported by reports that cardiac GLP-1R expression may be less ubiquitous than previously thought and the persistence of liraglutide-induced cardioprotection in mice with cardiomyocyte-specific GLP-1R deletion [ 41, 44], suggesting that the cardiac actions of GLP-1 may be mediated by an alternative cell type.
