Functional defects in the external and internal thin gates of the γ-aminobutyric acid (GABA) transporter GAT-1 can compensate each other

Assaf Ben-Yona; Baruch I. Kanner

doi:10.1074/jbc.M112.430215

Functional defects in the external and internal thin gates of the γ-aminobutyric acid (GABA) transporter GAT-1 can compensate each other

Assaf Ben-Yona
, Baruch I. Kanner^*

^*Corresponding author for this work

Institute for Medical Research Israel-Canada (IMRIC)

Research output: Contribution to journal › Article › peer-review

24 Scopus citations

Abstract

Background: Mutations in "thin" extra-and intracellular gates of GAT-1 impair gating and transport. Results: Transport activity of extracellular gate mutant can be rescued by its intracellular counterpart. Conclusion: A functional interaction of the external and internal gates of GAT-1 is essential for transport. Significance: The new insights into GAT-1 gating may be relevant for other transporters.

Original language	English
Pages (from-to)	4549-4556
Number of pages	8
Journal	Journal of Biological Chemistry
Volume	288
Issue number	7
DOIs	https://doi.org/10.1074/jbc.M112.430215
State	Published - 15 Feb 2013

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10.1074/jbc.M112.430215

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AB - Background: Mutations in "thin" extra-and intracellular gates of GAT-1 impair gating and transport. Results: Transport activity of extracellular gate mutant can be rescued by its intracellular counterpart. Conclusion: A functional interaction of the external and internal gates of GAT-1 is essential for transport. Significance: The new insights into GAT-1 gating may be relevant for other transporters.

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Functional defects in the external and internal thin gates of the γ-aminobutyric acid (GABA) transporter GAT-1 can compensate each other

Abstract

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