In ischemic stroke, synaptic NMDAR activation and Ca2+ influx activate the Ras/extracellular signal-regulated kinase (ERK) signaling pathway and nuclear Ca2+/calmodulin-dependent protein kinases, which in turn phosphorylate and activate cAMP-response element-binding protein (CREB). Activated CREB upregulates brain-derived neurotrophic factor (BDNF) activity and promotes the expression of numerous pro-neuronal survival genes. In conclusion, BDNF and the upstream CREB signaling pathway play a crucial role in promoting cell proliferation and survival, and preventing acute cerebral ischemic damage. The NR2A-CREB-BDNF-TrkB signaling pathway is a key target for actionable ischemic stroke therapy.
Fig. 1. Synaptic activity mediates prolonged neuronal survival via a positive feedback loop between CREB and BDNF. (Lai et al., 2014)
At Ace Therapeutics, we specialize in analyzing the NR2A-CREB-BDNF signaling pathway in stroke. We aim to help our clients discover and validate effective targets to protect neurons from post-ischemic stroke excitotoxicity by promoting the NR2A-CREB-BDNF-TrkB signaling pathway.
Our team of experienced researchers and scientists conducts comprehensive analyses using state-of-the-art techniques to elucidate the role of NR2A-CREB-BDNF signaling in stroke and develop potential therapeutic targets. Our research focuses on the following targets:
NMDAR- NR2A | Calmodulin kinase IV (CaMKIV) | ERK | CREB | Activating transcription factor 3 (ATF3) |
BDNF | TrkB-FL | MAPK | PI3K/Akt | PLCy |
With our expertise, state-of-the-art facilities, and collaborative approach, Ace Therapeutics is committed to helping customers discover and validate effective targets to target neuro-excitotoxicity in stroke. If you are interested in our services, please do not hesitate to contact us!
Ace Therapeutics is a global leading provider of stroke research services. We are committed to accelerating progress in stroke research and drug development.