Evidence map›Paper›PMID 29382685›Full record

ArticleJournal of the American Society of Nephrology : JASN2018

Proteomic Profiling Reveals the Transglutaminase-2 Externalization Pathway in Kidneys after Unilateral Ureteric Obstruction.

Giulia Furini, Nina Schroeder, Linghong Huang, David Boocock, Alessandra Scarpellini, Clare Coveney, Elisa Tonoli, Raghavendran Ramaswamy, Graham Ball, Claudia Verderio and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  17. Collagen VII maintains proteostasis in dermal fibroblasts by scaffolding TANGO1 cargo.Matrix biology : journal of the International Society for Matrix Biology · 2022
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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

12 authors at 3 institutions in 2 countries.

Giulia FuriniSchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom.
Nina SchroederSchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom.
Linghong HuangAcademic Nephrology Unit, Sheffield Kidney Institute, University of Sheffield, Sheffield, United Kingdom.
David BoocockJohn van Geest Cancer Research Centre, Nottingham Trent University, Nottingham, United Kingdom; and.
Alessandra ScarpelliniSchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom.
Clare CoveneyJohn van Geest Cancer Research Centre, Nottingham Trent University, Nottingham, United Kingdom; and.
Elisa TonoliSchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom.
Raghavendran RamaswamySchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom.
Graham BallJohn van Geest Cancer Research Centre, Nottingham Trent University, Nottingham, United Kingdom; and.
Claudia VerderioNational Research Council, Institute of Neuroscience, Milan, Italy.
Timothy S JohnsonAcademic Nephrology Unit, Sheffield Kidney Institute, University of Sheffield, Sheffield, United Kingdom.
Elisabetta A M VerderioSchool of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom; elisabetta.verderio-edwards@ntu.ac.uk.ORCID 0000-0002-7333-3549
Nottingham Trent University · GBSheffield Kidney Institute · GBNational Research Council · IT

Funding

Wellcome Trust
6 · The paper itself

Abstract

Increased export of transglutaminase-2 (TG2) by tubular epithelial cells (TECs) into the surrounding interstitium modifies the extracellular homeostatic balance, leading to fibrotic membrane expansion. Although silencing of extracellular TG2 ameliorates progressive kidney scarring in animal models of CKD, the pathway through which TG2 is secreted from TECs and contributes to disease progression has not been elucidated. In this study, we developed a global proteomic approach to identify binding partners of TG2 responsible for TG2 externalization in kidneys subjected to unilateral ureteric obstruction (UUO) using TG2 knockout kidneys as negative controls. We report a robust and unbiased analysis of the membrane interactome of TG2 in fibrotic kidneys relative to the entire proteome after UUO, detected by SWATH mass spectrometry. The data have been deposited to the ProteomeXchange with identifier PXD008173. Clusters of exosomal proteins in the TG2 interactome supported the hypothesis that TG2 is secreted by extracellular membrane vesicles during fibrosis progression. In established TEC lines, we found TG2 in vesicles of both endosomal (exosomes) and plasma membrane origin (microvesicles/ectosomes), and TGF-

Indexed as

Aniline CompoundsAnimalsBenzylidene CompoundsCell-Derived MicroparticlesCell LineEnzyme InhibitorsEpithelial CellsExosomesFibrosisGTP-Binding ProteinsHumansKidneyKidney TubulesMiceMice, KnockoutProtein Glutamine gamma Glutamyltransferase 2Aniline CompoundsBenzylidene CompoundsEnzyme InhibitorsGTP-Binding ProteinsGW 4869Protein Glutamine gamma Glutamyltransferase 2Sdc4 protein, mouseSdc4 protein, ratSphingomyelin PhosphodiesteraseSyndecan-4Tgfb1 protein, mouseTgfb1 protein, ratTgm2 protein, ratTransforming Growth Factor beta1Transglutaminaseschronic kidney diseaseextracellular vesiclesfibrosisinteractometransglutaminaseUUO

Identifiers

PMID29382685
PMCPMC5827594
OpenAlexW2786950932

What OpenQuestion holds

Textmetadata
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.