Evidence map›Paper›PMID 29197584›Full record

ArticleMolecular and cellular neurosciences2018

Depletion of transglutaminase 2 in neurons alters expression of extracellular matrix and signal transduction genes and compromises cell viability.

Laura Yunes-Medina, Alex Paciorkowski, Yan Nuzbrokh, Gail V W Johnson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 17 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

4 authors at 2 institutions in 1 country.

Laura Yunes-MedinaDepartment of Neuroscience, University of Rochester, 601 Elmwood Ave, Box 603, Rochester, NY 14642, United States. Electronic address: laura_yunes-medina@urmc.rochester.edu.
Alex PaciorkowskiDepartment of Neuroscience, University of Rochester, 601 Elmwood Ave, Box 603, Rochester, NY 14642, United States; Department of Neurology, University of Rochester, 601 Elmwood Ave, Box 603, Rochester, NY 14642, United States; Department of Pediatrics, University of Rochester Medical Center, 601 Elmwood Ave, Box 603, Rochester, NY 14642, United States; Department Biomedical Genetics, University of Rochester Medical Center, 601 Elmwood Ave, Box 604, Rochester, NY 14642, United States. Electronic address: Alex_Paciorkowski@urmc.rochester.edu.
Yan NuzbrokhDepartment of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Box 604, Rochester, NY 14642, United States. Electronic address: yn2374@gmail.com.
Gail V W JohnsonDepartment of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Box 604, Rochester, NY 14642, United States; Department of Pharmacology and Physiology, University of Rochester Medical Center, 601 Elmwood Ave, Box 604, Rochester, NY 14642, United States. Electronic address: gail_johnsonvoll@urmc.rochester.edu.
University of Rochester · USUniversity of Rochester Medical Center · US

Funding

The attenuation of ischemic injury by transglutaminase 2R01NS065825 · NINDS · UNIVERSITY OF ROCHESTER · PI JOHNSON, GAIL V. W. · 2011 to 2015
$1.8M
Biology of developmental encephalopathies presenting with infantile spasmsK08NS078054 · NINDS · UNIVERSITY OF ROCHESTER · PI PACIORKOWSKI, ALEXANDER R · 2013 to 2017
$779k
NINDS NIH HHS K08 NS078054NINDS NIH HHS R01 NS065825
6 · The paper itself

Abstract

The protein transglutaminase 2 (TG2) has been implicated as a modulator of neuronal viability. TG2's role in mediating cell survival processes has been suggested to involve its ability to alter transcriptional events. The goal of this study was to examine the role of TG2 in neuronal survival and to begin to delineate the pathways it regulates. We show that depletion of TG2 significantly compromises the viability of neurons in the absence of any stressors. RNA sequencing revealed that depletion of TG2 dysregulated the expression of 86 genes with 59 of these being upregulated. The genes that were upregulated by TG2 knockdown were primarily involved in extracellular matrix function, cell signaling and cytoskeleton integrity pathways. Finally, depletion of TG2 significantly reduced neurite length. These findings suggest for the first time that TG2 plays a crucial role in mediating neuronal survival through its regulation of genes involved in neurite length and maintenance.

Indexed as

AnimalsCells, CulturedCell SurvivalExtracellular MatrixFemaleGene ExpressionGTP-Binding ProteinsHEK293 CellsHumansNeuritesNeuronsPregnancyProtein Glutamine gamma Glutamyltransferase 2RatsRats, Sprague-DawleySignal TransductionGTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2Tgm2 protein, ratTransglutaminasesCell survivalNeurite lengthNeuronsRNA sequencingTransglutaminase

Identifiers

PMID29197584
PMCPMC5736014
OpenAlexW2768134330

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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.