Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na+ channel dynamics in human neurons
1.2, a voltage-gated sodium channel encoded by SCN2A, which displays aberrant subcellular distribution in XPO7 LoF neurons. Together, these findings position XPO7 as a critical regulator of neuronal excitability and connectivity, linking channelopathy to cellular phenotypes relevant to schizophrenia pathophysiology.
Authors
- Morgan Sheng (ORCID: https://orcid.org/0000-0002-8703-5366)
- Jen Q. Pan (ORCID: https://orcid.org/0000-0003-0767-086X)
- Erkin Kurganov (ORCID: https://orcid.org/0000-0003-4921-9161)
- Philipp Hornauer (ORCID: https://orcid.org/0000-0003-2265-6679)
- Ralda Nehme (ORCID: https://orcid.org/0000-0001-7215-3311)
- Yin Wang (ORCID: https://orcid.org/0000-0002-8137-7496)
- 林饶洲
- Lei Cui (ORCID: https://orcid.org/0009-0007-3679-4569)
- Andreas Hierlemann
- Derek Hawes
Institutions
- Broad Institute (US)
- ETH Zurich (CH)
Publication Details
- Journal
- Molecular Psychiatry
- Published
- 2026-04-15
- DOI
- https://doi.org/10.1038/s41380-026-03587-3
- Primary Topic
- Ion channel regulation and function
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Stanley Center for Psychiatric Research, Broad Institute
- National Institute of Mental Health