OSCR

ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.

Overview

Authors: Yi-Heng Hao1, Nofit Borenstein-Auerbach1, Anthony Grichuk1, Li Li1, M Carmen Lafita-Navarro1, Shun Fang1, Pedro A Nogueira1, Jiwoong Kim2, Lin Xu2,3, Jerry W Shay1,4, Maralice Conacci-Sorrell1,4,5
  1. Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA
  2. Department of Population & Data Sciences, Quantitative Biomedical Research Center, Peter O’Donnell Jr. School of Public Health, Dallas, TX 75390 USA
  3. Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA
  4. Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA
  5. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA
Journal: Cell communication and signaling : CCS, volume 24, issue 1, article 363
Dates: received 12 January 2026; accepted 26 April 2026; published online 1 May 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1186/s12964-026-02920-1 · PMID 42063073 · PMCID PMC13281552 · OpenAlex W7159594792
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), mouse (organism), other condition (population), cellular / molecular (subfield)
Methods: Statistics, Evoked potentials
Keywords: ARNT2, Glioblastoma, Differentiation, Stemness, MYC
MeSH: Aryl Hydrocarbon Receptor Nuclear Translocator*, Basic Helix-Loop-Helix Proteins*, Brain Neoplasms*, Glioblastoma*, Neurons*, Animals, Cell Differentiation, Cell Line, Tumor, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Mice, Proto-Oncogene Proteins c-myc (* major topic)
Topic: Glioma Diagnosis and Treatment (Genetics, Medicine), according to OpenAlex
Funding: NCI NIH HHS (P30 CA142543, R01 CA245548); NIGMS NIH HHS (R01 GM145744)
Citations: not cited yet (Europe PMC); 64 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

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

Data availability statement

The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

  • no repository, dataset or request procedure was recognized in it

Read it in the paper: doi.org/10.1186/s12964-026-02920-1.

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, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 11 authors, 5 keywords, 13 MeSH terms, 2 funders, 64 references.

Cite

This paper

Hao, Y.-H., Borenstein-Auerbach, N., Grichuk, A., Li, L., Lafita-Navarro, M. C., Fang, S., Nogueira, P. A., Kim, J., Xu, L., Shay, J. W., & Conacci-Sorrell, M. (2026). ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth. Cell communication and signaling : CCS, 24(1), 363. https://doi.org/10.1186/s12964-026-02920-1

BibTeX

@article{hao2026arnt2,
author = {Hao, Yi-Heng and Borenstein-Auerbach, Nofit and Grichuk, Anthony and Li, Li and Lafita-Navarro, M Carmen and Fang, Shun and Nogueira, Pedro A and Kim, Jiwoong and Xu, Lin and Shay, Jerry W and Conacci-Sorrell, Maralice},
title = {{ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth}},
journal = {Cell communication and signaling : CCS},
year = {2026},
month = may,
volume = {24},
number = {1},
pages = {363},
publisher = {BMC},
issn = {1478-811X},
doi = {10.1186/s12964-026-02920-1},
url = {https://doi.org/10.1186/s12964-026-02920-1},
pmid = {42063073},
pmcid = {PMC13281552}
}

RIS

TY - JOUR
AU - Hao, Yi-Heng
AU - Borenstein-Auerbach, Nofit
AU - Grichuk, Anthony
AU - Li, Li
AU - Lafita-Navarro, M Carmen
AU - Fang, Shun
AU - Nogueira, Pedro A
AU - Kim, Jiwoong
AU - Xu, Lin
AU - Shay, Jerry W
AU - Conacci-Sorrell, Maralice
TI - ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth
T2 - Cell communication and signaling : CCS
J2 - Cell Commun Signal
PY - 2026
DA - 2026/05/01
VL - 24
IS - 1
SP - 363
SN - 1478-811X
PB - BMC
DO - 10.1186/s12964-026-02920-1
UR - https://doi.org/10.1186/s12964-026-02920-1
LA - en
ER -

CSL-JSON

{
"id": "10.1186/s12964-026-02920-1",
"type": "article-journal",
"title": "ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth",
"container-title": "Cell communication and signaling : CCS",
"author": [
{
"family": "Hao",
"given": "Yi-Heng"
},
{
"family": "Borenstein-Auerbach",
"given": "Nofit"
},
{
"family": "Grichuk",
"given": "Anthony"
},
{
"family": "Li",
"given": "Li"
},
{
"family": "Lafita-Navarro",
"given": "M Carmen"
},
{
"family": "Fang",
"given": "Shun"
},
{
"family": "Nogueira",
"given": "Pedro A"
},
{
"family": "Kim",
"given": "Jiwoong"
},
{
"family": "Xu",
"given": "Lin"
},
{
"family": "Shay",
"given": "Jerry W"
},
{
"family": "Conacci-Sorrell",
"given": "Maralice"
}
],
"container-title-short": "Cell Commun Signal",
"volume": "24",
"issue": "1",
"page": "363",
"DOI": "10.1186/s12964-026-02920-1",
"PMID": "42063073",
"PMCID": "PMC13281552",
"ISSN": "1478-811X",
"publisher": "BMC",
"URL": "https://doi.org/10.1186/s12964-026-02920-1",
"language": "en",
"issued": {
"date-parts": [
[
2026,
5,
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/s41586-026-10295-z
AhR inhibition promotes axon regeneration via a stress-growth switch.
Journal: Nature
In common: other condition, mouse, cellular / molecular, 2 references
[2] doi:10.1038/s41398-026-03952-4 [code]
Perineuronal nets in cerebellar nuclei neurons orchestrate social behaviour via regulation of neuronal activity in circuits innervated by the cerebellum.
Journal: Translational psychiatry
In common: mouse, cellular / molecular, 2 references
[3] doi:10.1038/s41467-026-76587-0 [code]
Uncovering the signaling networks of disseminated glioblastoma cells in vivo with INSIGHT.
Journal: Nature communications
In common: other condition, mouse, cellular / molecular, 1 reference
[4] doi:10.1038/s41467-026-73802-w
Karyoptosis mediates cell death and neurodegeneration upon proteotoxic stress.
Journal: Nature communications
In common: other condition, mouse, cellular / molecular, 1 reference
[5] doi:10.1016/j.cell.2026.05.047 [code]
An emergent disease-associated motor neuron state precedes cell death in ALS.
Journal: Cell
In common: other condition, mouse, cellular / molecular, 1 reference
[6] doi:10.32604/or.2026.079221
Single-Cell Sequencing Reveals the Heterogeneity of Glioma and Identifies IGFBP2 as A Potential Therapeutic Target.
Journal: Oncology research
In common: other condition, mouse, cellular / molecular, 1 reference
[7] doi:10.1038/s42255-026-01508-w
Neuronal lipid droplets play a conserved and sex-biased role in maintaining whole-body energy homeostasis.
Journal: Nature metabolism
In common: mouse, cellular / molecular, 1 reference
[8] doi:10.1093/nar/gkag788 [code]
Neuronal activity-driven 3D chromatin dynamics in cortical pyramidal neurons depend on SATB2.
Journal: Nucleic acids research
In common: mouse, cellular / molecular, 1 reference
[9] doi:10.1172/jci.insight.199498
Distinct immune landscapes characterize highly versus minimally invasive brain metastases.
Journal: JCI insight
In common: other condition, mouse, 1 reference
[10] doi:10.1093/nar/gkag454 [code]
RegRegSEA: a web server for regulatory region set enrichment analysis of epigenomic data.
Journal: Nucleic acids research
In common: mouse, 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.

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.