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. 2017 Jan 5;7:40137. doi: 10.1038/srep40137

Table 2. Pathways enriched for M64.

Pathway PV CPV Time frame
Activation of NMDA receptor upon glutamate binding and postsynaptic events 1.73E-20 1.36E-18 mh
Glutamate Binding, Activation of AMPA Receptors and Synaptic Plasticity 3.54E-20 2.63E-18 smh
Trafficking of AMPA receptors 3.54E-20 2.63E-18 hd
Unblocking of NMDA receptor, glutamate binding and activation 4.17E-19 2.99E-17 mh
Depolarization of the Presynaptic Terminal Triggers the Opening of Calcium Channels 1.22E-15 6.96E-14 mh
Post-NMDA receptor activation events 1.62E-15 8.97E-14 mh
Ras activation upon Ca2+ influx through NMDA receptor 4.55E-14 2.27E-12 mh
CREB phosphorylation through the activation of CaMKII 5.85E-13 2.78E-11 mh
CREB phosphorylation through the activation of Ras 1.72E-12 7.69E-11 mh
Integration of energy metabolism 2.59E-11 1.01E-09 m
NCAM1 interactions 8.29E-10 2.84E-08 h
Rap1 signaling 6.49E-09 1.97E-07 hd
NCAM signaling for neurite out-growth 7.11E-08 1.84E-06 dwMy
PKA activation 2.28E-07 5.62E-06 mh
PKA activation in glucagon signaling 3.06E-07 7.43E-06 mh

Here, we describe 15 highly enriched pathways of M64. Most of these pathways are induced during the early stage of ischemic stroke (within minutes to hours (mh)). Two pathways are involved from hours to days (hd), and the pathway “NCAM signaling for neurite out-growth” can last for days, weeks, months or years (dwMy) (Table S6).