Engineering α4β2 nAChRs with reduced or increased nicotine sensitivity via selective disruption of consensus sites in the M3–M4 cytoplasmic loop of the α4 subunit

Author:

Biaggi-Labiosa Nilza M.,Avilés-Pagán EmirORCID,Caballero-Rivera Daniel,Báez-Pagán Carlos A.,Lasalde-Dominicci José A.

Funder

NIH

Publisher

Elsevier BV

Subject

Cellular and Molecular Neuroscience,Pharmacology

Reference29 articles.

1. Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc;Arany;Nephrol. Dial. Transplant.,2013

2. Pharmacology of nicotine: addiction and therapeutics;Benowitz;Annu. Rev. Pharmacol. Toxicol.,1996

3. Functional deactivation of the major neuronal nicotinic receptor caused by nicotine and a protein kinase C-dependent mechanism;Eilers;Mol. Pharmacol.,1997

4. Regulation of alpha4beta2 nicotinic receptor desensitization by calcium and protein kinase C;Fenster;Mol. Pharmacol.,1999

5. Upregulation of surface alpha4beta2 nicotinic receptors is initiated by receptor desensitization after chronic exposure to nicotine;Fenster;J. Neurosci. Off. J. Soc. Neurosci.,1999

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