Hyperekplexia mutation R271L of α1 glycine receptors potentiates allosteric interactions of nortropeines, propofol and glycine with [3H]strychnine binding-Reference-Cited by-同舟云学术

Hyperekplexia mutation R271L of α1 glycine receptors potentiates allosteric interactions of nortropeines, propofol and glycine with [3H]strychnine binding

Published:2008-01 Issue:1-2 Volume:52 Page:235-240
ISSN:0197-0186
Container-title:Neurochemistry International
language:en
Short-container-title:Neurochemistry International

Author:

Maksay Gábor,Bíró Tímea,Laube Bodo,Nemes Péter

Publisher

Elsevier BV

Subject

Cell Biology,Cellular and Molecular Neuroscience

Reference29 articles.

1. Defining the propofol binding site location on the GABAA receptor;Bali;Mol. Pharmcol.,2004

2. The interaction of general anaesthetics and neurosteroids with GABAA and glycine receptors;Belelli;Neurochem. Int.,1999

3. Glycine receptors: recent insights into their structural organisation and functional diversity;Betz;J. Neurochem.,2006

4. Allosteric modulation of glycine receptors is more efficacious for partial rather than full agonists;Bíró;Neurochem. Int.,2004

5. Potentiation of chloride responses to glycine by three 5-HT3 antagonists in rat spinal cord;Chesnoy-Marchais;Br. J. Pharmacol.,1996

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1. Disturbances of Ligand Potency and Enhanced Degradation of the Human Glycine Receptor at Affected Positions G160 and T162 Originally Identified in Patients Suffering from Hyperekplexia;Frontiers in Molecular Neuroscience;2015-12-22

2. The impact of human hyperekplexia mutations on glycine receptor structure and function;Molecular Brain;2014

3. 4-Chloropropofol enhances chloride currents in human hyperekplexic and artificial mutated glycine receptors;BMC Neurology;2012-09-24

4. Synthesis of heteroaromatic tropeines and heterogeneous binding to glycine receptors;Bioorganic & Medicinal Chemistry;2009-10

5. Different binding modes of tropeines mediating inhibition and potentiation of α1 glycine receptors;Journal of Neurochemistry;2009-06