GABAA receptor transmembrane amino acids are critical for alcohol action: disulfide cross-linking and alkyl methanethiosulfonate labeling reveal relative location of binding sites
Version of Record online: 28 OCT 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 128, Issue 3, pages 363–375, February 2014
How to Cite
J. Neurochem. (2014) 128, 363–375.
- Issue online: 21 JAN 2014
- Version of Record online: 28 OCT 2013
- Accepted manuscript online: 4 OCT 2013 01:28AM EST
- Manuscript Accepted: 30 SEP 2013
- Manuscript Revised: 26 SEP 2013
- Manuscript Received: 10 SEP 2013
- National Institutes of Health. Grant Number: AA06399
Figure S1. Representative tracing of currents through a receptor during the redox protocol. GABA responses were induced with the concentration that produced half the maximal response (EC50) for each mutant (see Table S1).
Figure S2. Comparison between wild-type and Cys-less α1β2γ2 GABAAR.
Figure S3. Concentration-response curves for single and double mutants in α and β subunits in a Cys-less background.
Figure S4. Concentration-response curves for double mutants in β subunits in a Cys-less background.
Figure S5. GABA-induced responses after DTT and Cu++/:phenanthroline application in single mutants (EC50 GABA was used).
Figure S6. Single cysteine mutations and drug effects.
Table S1. GABA concentration-response curves parameters.
Table S2. Cα-Cα distances between the cysteine pairs studied, according to the model.
Table S3. Drug binding to locations in transmembrane regions (TM) of ligand-gated ion channels.
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