PrP<sup>C</sup>-facilitated cell signaling activates phospholipase Cɣ1 and triggers an Arc/Arg3.1 response in mouse and iPSC-derived human neurons.
Overview
- Department of Pathology, University of California, San Diego, La Jolla, CA 92093, USA
- Department of Integrative Structural and Computational Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
- Department of Neurology, Weill Institute for Neurosciences, Memory and Aging Center, University of California, San Francisco, San Francisco, CA 94158, USA
- Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
- Department of Pathology, Immunology, and Microbiology, University of California, Davis, Davis, CA 95616, USA
Abstract
Synapse loss is an early feature of prion disease, yet the underlying drivers are poorly understood. We recently found evidence of neuronal hyperactivity and synaptic loss in prion-infected mice. Herein, we identified increased Arc/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
The paper's code and data availability statement is in the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data and code availability
• The data that support the findings of this study are either provided as supplemental information, deposited in publicly available repositories (RNA-seq data available from the GEO depository, accession number GSE327330; proteomic data available from the ProteomExchange depository, accession number PXD068396 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
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 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 11 authors, 10 keywords, 11 MeSH terms, 3 funders, 100 references, 11 RRIDs.
Cite
This paper
Ojeda-Juarez, D., Funk, G., McClatchy, D. B., Richards, E., Rajic, A. J., Soldau, K., Geschwind, M. D., Chen, X., Yates, J. R., Gonias, S. L., & Sigurdson, C. J. (2026). PrP&
BibTeX
@article{ojedajuarez2026
author = {Ojeda-Juarez, Daniel and Funk, Gail and McClatchy, Daniel B. and Richards, Emily and Rajic, Alexander J. and Soldau, Katrin and Geschwind, Michael D. and Chen, Xu and Yates, John R. and Gonias, Steven L. and Sigurdson, Christina J.},
title = {{PrP\&
journal = {Stem cell reports},
year = {2026},
month = may,
volume = {21},
number = {6},
pages = {102924},
publisher = {Elsevier},
issn = {2213-6711},
doi = {10.1016/
url = {https://
pmid = {42140197},
pmcid = {PMC13261956}
}
RIS
TY - JOUR
AU - Ojeda-Juarez, Daniel
AU - Funk, Gail
AU - McClatchy, Daniel B.
AU - Richards, Emily
AU - Rajic, Alexander J.
AU - Soldau, Katrin
AU - Geschwind, Michael D.
AU - Chen, Xu
AU - Yates, John R.
AU - Gonias, Steven L.
AU - Sigurdson, Christina J.
TI - PrP&
T2 - Stem cell reports
J2 - Stem Cell Reports
PY - 2026
DA - 2026/
VL - 21
IS - 6
SP - 102924
SN - 2213-6711
PB - Elsevier
DO - 10.1016/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1016/
"type": "article-journal",
"title": "PrP&
"container-title": "Stem cell reports",
"author": [
{
"family": "Ojeda-Juarez",
"given": "Daniel"
},
{
"family": "Funk",
"given": "Gail"
},
{
"family": "McClatchy",
"given": "Daniel B."
},
{
"family": "Richards",
"given": "Emily"
},
{
"family": "Rajic",
"given": "Alexander J."
},
{
"family": "Soldau",
"given": "Katrin"
},
{
"family": "Geschwind",
"given": "Michael D."
},
{
"family": "Chen",
"given": "Xu"
},
{
"family": "Yates",
"given": "John R."
},
{
"family": "Gonias",
"given": "Steven L."
},
{
"family": "Sigurdson",
"given": "Christina J."
}
],
"container-title-short":
"volume": "21",
"issue": "6",
"page": "102924",
"DOI": "10.1016/
"PMID": "42140197",
"PMCID": "PMC13261956",
"ISSN": "2213-6711",
"publisher": "Elsevier",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
5,
14
]
]
}
}
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:10.1371/journal.ppat.1014314
- Chemo-omic pipeline enables discovery of prion synaptotoxic pathways and inhibitory drugs.Journal: PLoS pathogensIn common: genetics / omics, other condition, mouse, 1 other category, 4 references
- [2] doi:10.1002/adhm.202504889 [code]
- Mapping the Cerebral Organoid Landscape: A Systematic Review of Preclinical 3D Models in Neuroscience.Journal: Advanced healthcare materialsIn common: other condition, 4 references
- [3] doi:10.1038/s41467-026-75895-9
- Distinct Filament Conformation for Receptor-Bound Amyloid-β from Alzheimer's Disease Brain.Journal: Nature communicationsIn common: Alzheimer's / dementia, other condition, cellular / molecular, 3 references
- [4] doi:10.1080/19336896.2026.2710965
- Epigenetic changes associated with the progression of prion disease in Syrian hamsters (&
lt;i& gt;Mesocricetus auratus& lt;/ i& gt;). Journal: PrionIn common: genetics / omics, other condition, cellular / molecular, 3 references - [5] doi:10.1093/nar/gkag287 [code]
- Divalent siRNA for prion disease.Journal: Nucleic acids researchIn common: other condition, mouse, 3 references
- [6] doi:10.1038/s41467-026-73003-5 [code]
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Journal: Nature communicationsIn common: other condition, mouse, cellular / molecular, 3 references
- [7] doi:10.1111/ejn.70480 [code]
- Astrocyte Proximity Protects Synapses From Human Amyloid-Beta Induced Degeneration in a Mouse Ex Vivo Model of Early Alzheimer's Disease.Journal: The European journal of neuroscienceIn common: Alzheimer's / dementia, mouse, cellular / molecular, 3 references
- [8] doi:10.1038/s41467-026-69866-3 [code]
- Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.Journal: Nature communicationsIn common: Alzheimer's / dementia, mouse, cellular / molecular, 3 references
- [9] doi:10.1186/s13024-026-00936-2
- Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology.Journal: Molecular neurodegenerationIn common: Alzheimer's / dementia, mouse, cellular / molecular, 2 references
- [10] doi:10.1038/s41467-026-74202-w [code]
- Repetitive neuronal activation regulates cellular maturation state via nuclear reprogramming.Journal: Nature communicationsIn common: mouse, cellular / molecular, 2 references
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.