Evidence map›Paper›PMID 34360011›Full record

ReviewCells2021

Role of Transglutaminase 2 in Cell Death, Survival, and Fibrosis.

Hideki Tatsukawa, Kiyotaka Hitomi

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
8.7field-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

72 citing papers in PubMed, 91 citations in OpenAlex.

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  19. The cross-linking activity of transglutaminase 2 drives α-Synuclein pathology in synucleinopathy models.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  20. Article

12 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Hideki TatsukawaCellular Biochemistry Laboratory, Graduate School of Pharmaceutical Sciences, Nagoya University, Tokai National Higher Education and Research System, Nagoya 464-8601, Aichi, Japan.ORCID 0000-0003-0059-9677
Kiyotaka HitomiCellular Biochemistry Laboratory, Graduate School of Pharmaceutical Sciences, Nagoya University, Tokai National Higher Education and Research System, Nagoya 464-8601, Aichi, Japan.
Tokai National Higher Education and Research System

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transglutaminase 2 (TG2) is a ubiquitously expressed enzyme catalyzing the crosslinking between Gln and Lys residues and involved in various pathophysiological events. Besides this crosslinking activity, TG2 functions as a deamidase, GTPase, isopeptidase, adapter/scaffold, protein disulfide isomerase, and kinase. It also plays a role in the regulation of hypusination and serotonylation. Through these activities, TG2 is involved in cell growth, differentiation, cell death, inflammation, tissue repair, and fibrosis. Depending on the cell type and stimulus, TG2 changes its subcellular localization and biological activity, leading to cell death or survival. In normal unstressed cells, intracellular TG2 exhibits a GTP-bound closed conformation, exerting prosurvival functions. However, upon cell stimulation with Ca

Indexed as

Alternative SplicingAminoacyltransferasesAnimalsCalciumCarbon-Nitrogen LyasesCell DeathCell SurvivalFibrosisGene ExpressionGTP-Binding ProteinsGuanosine TriphosphateHumansInflammationIsoenzymesMacrophagesPhagocytosisAminoacyltransferasesCalciumCarbon-Nitrogen LyasesGTP-Binding ProteinsGuanosine TriphosphateIsoenzymesisopeptidaseProtein Disulfide-IsomerasesProtein Glutamine gamma Glutamyltransferase 2transamidasesTransglutaminasescell deathcell survivalcrosslinkingfibrosismacrophage activationTG2transglutaminase

Identifiers

PMID34360011
PMCPMC8307792
OpenAlexW3183458763

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.