Evidence map›Paper›PMID 34560191›Full record

ArticleNeuroscience letters2021

Developmentally upregulated transcriptional elongation factor a like 3 suppresses axon regeneration after optic nerve injury.

Agnieszka Lukomska, Juhwan Kim, Bruce A Rheaume, Jian Xing, Alexela Hoyt, Emmalyn Lecky, Tyler Steidl, Ephraim F Trakhtenberg

Open access · hybridAbstract read
In one paragraph

Article in Neuroscience letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Agnieszka LukomskaDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Juhwan KimDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Bruce A RheaumeDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Jian XingDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Alexela HoytDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Emmalyn LeckyDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Tyler SteidlDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA.
Ephraim F TrakhtenbergDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06030, USA. Electronic address: trakhtenberg@uchc.edu.
University of Connecticut · US

Funding

Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacityR01EY029739 · NEI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI TRAKHTENBERG, FELIKS EPHRAIM · 2019 to 2023
$2.1M
NEI NIH HHS R01 EY029739
6 · The paper itself

Abstract

Projection neurons of the mammalian central nervous system (CNS) do not spontaneously regenerate axons which have been damaged by an injury or disease, often leaving patients with permanent disabilities that affect motor, cognitive, or sensory functions. Although several molecular targets which promote some extent of axon regeneration in animal models have been identified, the resulting recovery is very limited, and the molecular mechanisms underlying the axonal regenerative failure in the CNS are still poorly understood. One of the most studied targets for axon regeneration in the CNS is the mTOR pathway. A number of developmentally regulated genes also have been found to play a role in CNS axon regeneration. Here, we found that Transcriptional Elongation Factor A Like 3 (Tceal3), belonging to the Bex/Tceal transcriptional regulator family, which also modulates the mTOR pathway, is developmentally upregulated in retinal ganglion cell (RGCs) projection CNS neurons, and suppresses their capacity to regenerate axons after injury.

Indexed as

AxonsNerve RegenerationOptic Nerve InjuriesTranscriptional Elongation FactorsAnimalsGene Expression Regulation, DevelopmentalGene Knockdown TechniquesHumansMiceRetinal Ganglion CellsSignal TransductionTOR Serine-Threonine KinasesUp-RegulationmTOR protein, mouseTceal3 protein, mouseTOR Serine-Threonine KinasesTranscriptional Elongation FactorsAxon regenerationOptic nerveRetinal ganglion cellRNA-seq

Identifiers

PMID34560191
PMCPMC8572158
OpenAlexW3201367159

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.