p(HGNC:MAPK1, pmod(Ph))

Entity

Name

MAPK1

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Whatever the mechanism of uptake, it is interesting to note that the signaling pathways evoked by the accumulation of intracellular Abeta resemble those evoked by extracellularly applied Abeta: transgenic rats overexpressing Abeta intraneuronally display elevated levels of phosphorylated ERK2 (Echeverria et al., 2004), as do rat hippocampal slices in response to bath-applied Abeta (Dineley et al., 2001). Again, bath-applied Abeta causes an increase in BAX and a decrease in BCL2 expression in neurons or neuronlike cell lines (Koriyama et al., 2003; Clementi et al., 2006). PubMed:19293145

In studies on SH-SY5Y cells and cultured rat hippocampal neurons, nicotine, acting through alpha7 nAChRs, results in the activation of ERK-1/2 pathways dependent upon calcium and protein kinase A (Dajas-Bailador et al., 2002b). In addition, the alpha7-specific agonist GTS-21 promotes ERK-1/2 phosphorylation, but not that of c-jun N-terminal kinase (JNK) or p38 (Ren et al., 2005). PubMed:19293145

Furthermore, nicotinic activation of ERK-1/2 promotes survival of cultured murine spinal cord neurons, and the blocking of ERK-1 prevents nicotine’s antiapoptotic action (Toborek et al., 2007). Likewise, the alpha7-specific agonist A-582941 induces phosphorylation of ERK-1/2 in PC12 cells and in mouse brain, and this is completely blocked by the mitogen-activated protein kinase 1 inhibitor SL327 (Bitner et al., 2007). PubMed:19293145