The Role of Disulfide Bonds in the GluN1 Subunit in the Early Trafficking and Functional Properties of GluN1/GluN2 and GluN1/GluN3 NMDA Receptors.
Overview
- Institute of Experimental Medicine of the Czech Academy of Sciences, Prague 4 14220, Czech Republic
- Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea
- Neuroscience Research Institute, Medical Research Center, Seoul National University, Seoul 03080, South Korea
Abstract
N-Methyl-d-aspartate receptors (NMDARs) are ionotropic glutamate receptors essential for excitatory neurotransmission. Previous studies proposed the existence of four disulfide bonds in the GluN1 subunit; however, their role in NMDAR trafficking remains unclear. Our study first confirmed the existence of four disulfide bonds in the GluN1 subunit using biochemistry in human embryonic kidney 293T (HEK293T) cells. Disrupting the individual disulfide bonds by serine replacements produced the following surface expression trend for GluN1/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- zenodo:14794644, at Zenodo; found in DataCite
- zenodo:14794645, at Zenodo; found in DataCite
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 2, 28 September 2026
- Funding: added Korea Dementia Research Center: RS-2024-00332875; Ministerstvo Školství, Mládeže a Tělovýchovy: LM2023050, LX22NPO5107, CZ.02.01.01/00/ 22_008/0004562
Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 14 authors, 6 keywords, 14 MeSH terms, 65 references, 20 RRIDs.
Cite
This paper
Netolicky, J., Lee, S., Zahumenska, P., Kolcheva, M., Misiachna, A., Rehakova, K., Kortus, S., Song, J.-m., Hemelikova, K., Langore, E., Doderović, J., Ladislav, M., Suh, Y. H., & Horak, M. (2026). The Role of Disulfide Bonds in the GluN1 Subunit in the Early Trafficking and Functional Properties of GluN1/
BibTeX
@article{netolicky2026ro
author = {Netolicky, Jakub and Lee, Seungha and Zahumenska, Petra and Kolcheva, Marharyta and Misiachna, Anna and Rehakova, Kristyna and Kortus, Stepan and Song, Jae-man and Hemelikova, Katarina and Langore, Emily and Doderović, Jovana and Ladislav, Marek and Suh, Young Ho and Horak, Martin},
title = {{The Role of Disulfide Bonds in the GluN1 Subunit in the Early Trafficking and Functional Properties of GluN1/
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
year = {2026},
month = apr,
volume = {46},
number = {13},
pages = {e0409252026},
publisher = {Society for Neuroscience},
issn = {0270-6474},
doi = {10.1523/
url = {https://
pmid = {41735054},
pmcid = {PMC13064811}
}
RIS
TY - JOUR
AU - Netolicky, Jakub
AU - Lee, Seungha
AU - Zahumenska, Petra
AU - Kolcheva, Marharyta
AU - Misiachna, Anna
AU - Rehakova, Kristyna
AU - Kortus, Stepan
AU - Song, Jae-man
AU - Hemelikova, Katarina
AU - Langore, Emily
AU - Doderović, Jovana
AU - Ladislav, Marek
AU - Suh, Young Ho
AU - Horak, Martin
TI - The Role of Disulfide Bonds in the GluN1 Subunit in the Early Trafficking and Functional Properties of GluN1/
T2 - The Journal of neuroscience : the official journal of the Society for Neuroscience
J2 - J Neurosci
PY - 2026
DA - 2026/
VL - 46
IS - 13
SP - e0409252026
SN - 0270-6474
PB - Society for Neuroscience
DO - 10.1523/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1523/
"type": "article-journal",
"title": "The Role of Disulfide Bonds in the GluN1 Subunit in the Early Trafficking and Functional Properties of GluN1/
"container-title": "The Journal of neuroscience : the official journal of the Society for Neuroscience",
"author": [
{
"family": "Netolicky",
"given": "Jakub"
},
{
"family": "Lee",
"given": "Seungha"
},
{
"family": "Zahumenska",
"given": "Petra"
},
{
"family": "Kolcheva",
"given": "Marharyta"
},
{
"family": "Misiachna",
"given": "Anna"
},
{
"family": "Rehakova",
"given": "Kristyna"
},
{
"family": "Kortus",
"given": "Stepan"
},
{
"family": "Song",
"given": "Jae-man"
},
{
"family": "Hemelikova",
"given": "Katarina"
},
{
"family": "Langore",
"given": "Emily"
},
{
"family": "Doderović",
"given": "Jovana"
},
{
"family": "Ladislav",
"given": "Marek"
},
{
"family": "Suh",
"given": "Young Ho"
},
{
"family": "Horak",
"given": "Martin"
}
],
"container-title-short":
"volume": "46",
"issue": "13",
"page": "e0409252026",
"DOI": "10.1523/
"PMID": "41735054",
"PMCID": "PMC13064811",
"ISSN": "0270-6474",
"publisher": "Society for Neuroscience",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41594-026-01866-9 [code]
- Structural and mechanistic insights into gating and allosteric modulation of GluN1-GluN3A NMDA receptors.Journal: Nature structural & molecular biologyIn common: cellular / molecular, 5 references
- [2] doi:10.1186/s13023-025-04055-x
- GRIN2B-related neurodevelopmental disorders: genotype-phenotype correlations and therapeutic implicationsJournal: n/aIn common: genetics / omics, 4 references
- [3] doi:10.1016/j.isci.2026.117309 [code]
- Intracellular regulation of a serotonin-gated ion channel links receptor trafficking to memory.Journal: iScienceIn common: cellular / molecular, 2 references
- [4] doi:10.1126/sciadv.aee6579 [code]
- Dopamine D2 receptors bypass canonical signaling to directly tune NMDA receptor function and aversive learning.Journal: Science advancesIn common: cellular / molecular, 2 references
- [5] doi:10.3389/fncom.2026.1753444 [code]
- NMDA receptor kinetics drive distinct routes to chaotic firing in pyramidal neurons.Journal: Frontiers in computational neuroscienceIn common: cellular / molecular, 2 references
- [6] doi:10.1371/journal.pone.0350674
- Transcriptomic profile of the hippocampus of rat strains with contrasting nervous system excitability.Journal: PloS oneIn common: rat, genetics / omics, cellular / molecular, 1 reference
- [7] doi:10.31083/ap46200
- &
lt;i& gt;GRIA& lt;/ i& gt; Gene Expression in Schizophrenia: A Participant-Level Meta-Analysis. Journal: Alpha psychiatryIn common: genetics / omics, cellular / molecular, 1 reference - [8] doi:10.1126/sciadv.aee8648 [code]
- IoT-enabled wireless neural implant for chronic, programmable neuropharmacology and optogenetics.Journal: Science advancesIn common: rat, 1 reference
- [9] doi:10.1007/s12017-026-08935-8
- Subgroup-Specific Associations of GRIA Genes Encoding AMPA Glutamate Receptor Subunits with Patient Survival in Medulloblastoma.Journal: Neuromolecular medicineIn common: genetics / omics, cellular / molecular, 1 reference
- [10] doi:10.1038/s41467-026-73409-1
- Cryo-EM Structure of the TRPC1/
5 Heteromer Enables Design of Antidepressant and Anxiolytic Drug with Reduced Side Effects. Journal: Nature communicationsIn common: cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.