The Neuroprotective Effect of 2-(3-Pyridyl)-1-azabicyclo[3.2.2]nonane (TC-1698), a Novel α7 Ligand, Is Prevented through Angiotensin II Activation of a Tyrosine Phosphatase

@article{Marrero2004TheNE,
  title={The Neuroprotective Effect of 2-(3-Pyridyl)-1-azabicyclo[3.2.2]nonane (TC-1698), a Novel $\alpha$7 Ligand, Is Prevented through Angiotensin II Activation of a Tyrosine Phosphatase},
  author={Mario B. Marrero and Roger L. Papke and Balwinder Singh Bhatti and Se{\'a}n M Shaw and Merouane Bencherif},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2004},
  volume={309},
  pages={16 - 27}
}
We have recently provided evidence for nicotine-induced complex formation between the α7 nicotinic acetylcholine receptor (nAChR) and the tyrosine-phosphorylated enzyme Janus kinase 2 (JAK2) that results in subsequent activation of phosphatidylinositol-3-kinase (PI-3-K) and Akt. Nicotine interaction with the α7 nAChR inhibits Aβ (1-42) interaction with the same receptor, and the Aβ (1-42)-induced apoptosis is prevented through nicotine-induced activation of JAK2. These effects can be shown by… 

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Evidence is provided that nicotine stimulation of α7 nAChR transduces signals to phosphatidylinositol 3-kinase and Akt via Janus kinase 2 (JAK2) in a cascade, which results in neuroprotection, suggesting a pivotal role for JAK2.

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Evidence that nicotine stimulation of alpha7 nAChR transduces signals to phosphatidylinositol 3-kinase and Akt via Janus kinase 2 (JAK2) in a cascade, which results in neuroprotection is provided.

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