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Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na<sup>+</sup> channel dynamics in human neurons.

Overview

Authors: Lei Cui1, Erkin Kurganov1, Derek Hawes1, Philipp Hornauer2, Raozhou Lin1, Yining Wang1, Andreas Hierlemann2, Morgan Sheng1, Ralda Nehme1, Jen Q Pan1
  1. Stanley Center for Psychiatric Research, The Broad Institute of MIT and Harvard, 75 Ames Street, Cambridge, MA 02115 USA
  2. Department of Biosystems Science and Engineering, ETH Zürich, 4056 Basel, Switzerland
Institutions: Broad Institute (United States); Harvard University (United States); Stanley Center for Psychiatric Research; Massachusetts Institute of Technology (United States); ETH Zurich (Switzerland)
Journal: Molecular psychiatry, volume 31, issue 9, pages 4995-5013
Dates: received 21 July 2025; accepted 23 March 2026; published online 15 April 2026; in print 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1038/s41380-026-03587-3 · PMID 41986745 · PMCID PMC13441981 · OpenAlex W7154476375
Open access: hybrid, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), human (organism), schizophrenia / psychosis (population), cellular / molecular (subfield)
Methods: Spectral & time-frequency, Statistics, Smoothing, state filtering, decompositions, Evoked potentials, Machine learning, Single-unit activity, calcium imaging
Keywords: Stem cells, Schizophrenia, Neuroscience
MeSH: Karyopherins*, Receptors, Cytoplasmic and Nuclear*, Schizophrenia*, Genetic Predisposition to Disease, Humans, Induced Pluripotent Stem Cells, Loss of Function Mutation, NAV1.2 Voltage-Gated Sodium Channel, Neurons, Sodium Channels (* major topic)
Topic: Ion channel regulation and function (Molecular Biology, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) (MH131719, S10MH133644); NIMH NIH HHS (R01 MH131719, S10 MH133644, RF1 MH131719); Broad Institute | Stanley Center for Psychiatric Research, Broad Institute (Stanley Center) (RN)
Citations: not cited yet (Europe PMC); 59 references in the paper

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

Code

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Data

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Code and data availability statement

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Versions

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Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 10 authors, 3 keywords, 10 MeSH terms, 3 funders, 53 references.

Cite

This paper

Cui, L., Kurganov, E., Hawes, D., Hornauer, P., Lin, R., Wang, Y., Hierlemann, A., Sheng, M., Nehme, R., & Pan, J. Q. (2026). Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na<sup>+</sup> channel dynamics in human neurons. Molecular psychiatry, 31(9), 4995-5013. https://doi.org/10.1038/s41380-026-03587-3

BibTeX

@article{cui2026loss,
author = {Cui, Lei and Kurganov, Erkin and Hawes, Derek and Hornauer, Philipp and Lin, Raozhou and Wang, Yining and Hierlemann, Andreas and Sheng, Morgan and Nehme, Ralda and Pan, Jen Q},
title = {{Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na\<sup\>+\</sup\> channel dynamics in human neurons}},
journal = {Molecular psychiatry},
year = {2026},
month = apr,
volume = {31},
number = {9},
pages = {4995--5013},
publisher = {Springer Nature},
issn = {1359-4184},
doi = {10.1038/s41380-026-03587-3},
url = {https://doi.org/10.1038/s41380-026-03587-3},
pmid = {41986745},
pmcid = {PMC13441981}
}

RIS

TY - JOUR
AU - Cui, Lei
AU - Kurganov, Erkin
AU - Hawes, Derek
AU - Hornauer, Philipp
AU - Lin, Raozhou
AU - Wang, Yining
AU - Hierlemann, Andreas
AU - Sheng, Morgan
AU - Nehme, Ralda
AU - Pan, Jen Q
TI - Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na<sup>+</sup> channel dynamics in human neurons
T2 - Molecular psychiatry
J2 - Mol Psychiatry
PY - 2026
DA - 2026/04/15
VL - 31
IS - 9
SP - 4995
EP - 5013
SN - 1359-4184
PB - Springer Nature
DO - 10.1038/s41380-026-03587-3
UR - https://doi.org/10.1038/s41380-026-03587-3
LA - en
ER -

CSL-JSON

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