Human ARHGEF9 intellectual disability syndrome is phenocopied by a mutation that disrupts collybistin binding to the GABAA receptor α2 subunit

Authors

Dustin J. Hines, University of Nevada, Las Vegas
April Contreras, University of Nevada, Las Vegas
Betsua Garcia, University of Nevada, Las Vegas
Jeffrey S. Barker, University of Nevada, Las Vegas
Austin J. Boren, University of Nevada, Las Vegas
Cristelle Moufawad El Achlar, Boston Children's Hospital
Stephen J. Moss, Tufts University School of Medicine
Rochelle M. Hines, University of Nevada, Las Vegas

Document Type

Article

Publication Date

5-12-2022

Publication Title

Molecular Psychiatry

Volume

27

Issue

1275

Last page number:

1

Abstract

Enrichment of collybistin to parvalbumin positive clusters on the soma of pyramidal cells in mouse cortex. Collybistin (green) is strongly enriched at parvalbumin (red) clusters that surround the pyramidal cell soma. Collybistin remains enriched at the parvalbumin clusters on somas in the cortex of Gabra2-1 mice suggesting that collybistin is trafficked to these sites independent of interaction with the α2 subunit of GABAA receptors. For more information, please refer to the article by Hines et al. in this issue.

Controlled Subject

Animal psychology; Cerebral cortex

Disciplines

Behavior and Ethology

File Format

PDF

File Size

919 KB

Language

English

Rights

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Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

Repository Citation

Hines, D. J., Contreras, A., Garcia, B., Barker, J. S., Boren, A. J., El Achlar, C. M., Moss, S. J., Hines, R. M. (2022). Human ARHGEF9 intellectual disability syndrome is phenocopied by a mutation that disrupts collybistin binding to the GABAA receptor α2 subunit. Molecular Psychiatry, 27(1275),
http://dx.doi.org/10.1038/s41380-022-01559-x