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In the hearts, ER stress response has been shown to be activated in several pathological models including myocardial infarction, ischemia/reperfusion and pressure overload-induced hypertrophy [20], [21], [13], [22].
Recently, NF-κB signaling was found to be activated in several tissues with aging [ 42].
Recently, it has been reported that the Wnt pathway may be activated in several sarcomas [ 2- 5].
Wild-type p53 can be activated in several malignancies by treatment with nerve growth factor [ 29] or pharmacologic agents [ 30- 33], occurring through mechanisms sparing cells from the concomitant genotoxicity following chemotherapy.
In recent decades, the signalling pathways initiated by these effectors have been found to be activated in several human tumours and, consequently, PyV mT model systems continue to be employed in cancer research (reviewed extensively in [ 1]).
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For example, the PERK pathway is activated in several neurodegenerative diseases, in the presence or absence of activation of the other UPR pathways.
It is now clear that when animals are presented with a diet devoid of a single essential amino acid, the GCN2/eIF2α pathway is activated in several tissues.
Stat3 as mentioned earlier is activated in several human tumors, rendering them resistant to apoptotsis by regulating various anti-apoptotic proteins [31].
MET is activated in several tumour types and may be a promising therapeutic target.
The JNK pathway is activated in several models of brain injury and its inhibition confers neuroprotection.
In addition, autophagy is activated in several neurodegenerative diseases, including AD, and we found that γ-taxilin was depleted in the AD brains.
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