Evidence map›Paper›PMID 35906210›Full record

ArticleNature communications2022

Transcription factor network analysis identifies REST/NRSF as an intrinsic regulator of CNS regeneration in mice.

Yuyan Cheng, Yuqin Yin, Alice Zhang, Alexander M Bernstein, Riki Kawaguchi, Kun Gao, Kyra Potter, Hui-Ya Gilbert, Yan Ao, Jing Ou and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 65 citations in OpenAlex.

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  5. The conserved fibroblast growth factor receptor-based signaling is required for dendrite regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 1 country.

Yuyan Cheng *Program in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Yuqin Yin *Department of Neurosurgery, Boston Children's Hospital, Boston, MA, 02115, USA.
Alice ZhangProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Alexander M BernsteinDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Riki KawaguchiProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Kun GaoProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Kyra PotterProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Hui-Ya GilbertDepartment of Neurosurgery, Boston Children's Hospital, Boston, MA, 02115, USA.
Yan AoDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Jing OuProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Catherine J Fricano-KuglerProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Jeffrey L GoldbergByers Eye Institute and Wu Tsai Neuroscience Institute, Stanford University, Palo Alto, CA, 94305, USA.
Zhigang HeF.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA, 02115, USA.ORCID 0000-0001-6080-6880
Clifford J WoolfF.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA, 02115, USA.ORCID 0000-0002-6636-3897
Michael V SofroniewDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.ORCID 0000-0001-6075-0178
Larry I BenowitzDepartment of Neurosurgery, Boston Children's Hospital, Boston, MA, 02115, USA. larry.benowitz@childrens.harvard.edu.ORCID 0000-0002-0277-7222
Daniel H GeschwindProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA. dhg@mednet.ucla.edu.ORCID 0000-0003-2896-3450
University of California, Los Angeles · USBoston Children's Hospital · USStanford University · US

Funding

Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SCOTT Loren POMEROY, MUSTAFA SAHIN · 2021 to 2026
$9.4M
Injectable biomaterial depots to manipulate scar and foster axon growth after SCIR01NS084030 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SOFRONIEW, MICHAEL V · 2014 to 2023
$3.0M
Molecular Discovery for Optic Nerve RegenerationU01EY027261 · NEI · STANFORD UNIVERSITY · PI GOLDBERG, JEFFREY L, HUBERMAN, ANDREW D · 2016 to 2019
$3.0M
Shared multi-photon confocal microscopeS10OD016453 · OD · BOSTON CHILDREN'S HOSPITAL · PI CHEN, CHINFEI · 2013 to 2013
$495k
NEI NIH HHS U01 EY027261NICHD NIH HHS P50 HD105351NIH HHS S10 OD016453NINDS NIH HHS R01 NS084030
6 · The paper itself

Abstract

The inability of neurons to regenerate long axons within the CNS is a major impediment to improving outcome after spinal cord injury, stroke, and other CNS insults. Recent advances have uncovered an intrinsic program that involves coordinate regulation by multiple transcription factors that can be manipulated to enhance growth in the peripheral nervous system. Here, we use a systems genomics approach to characterize regulatory relationships of regeneration-associated transcription factors, identifying RE1-Silencing Transcription Factor (REST; Neuron-Restrictive Silencer Factor, NRSF) as a predicted upstream suppressor of a pro-regenerative gene program associated with axon regeneration in the CNS. We validate our predictions using multiple paradigms, showing that mature mice bearing cell type-specific deletions of REST or expressing dominant-negative mutant REST show improved regeneration of the corticospinal tract and optic nerve after spinal cord injury and optic nerve crush, which is accompanied by upregulation of regeneration-associated genes in cortical motor neurons and retinal ganglion cells, respectively. These analyses identify a role for REST as an upstream suppressor of the intrinsic regenerative program in the CNS and demonstrate the utility of a systems biology approach involving integrative genomics and bio-informatics to prioritize hypotheses relevant to CNS repair.

Indexed as

AxonsSpinal Cord InjuriesAnimalsMiceNerve RegenerationRE1-Silencing Transcription FactorRepressor ProteinsRetinal Ganglion CellsTranscription FactorsRE1-Silencing Transcription FactorRepressor ProteinsTranscription Factors

Identifiers

PMID35906210
PMCPMC9338053
OpenAlexW4288698497

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.