Evidence map›Paper›PMID 29897613›Full record

ArticleFEBS letters2018

Enhanced expression of thioredoxin-interacting-protein regulates oxidative DNA damage and aging.

Tina Oberacker, Jörg Bajorat, Sabine Ziola, Anne Schroeder, Daniel Röth, Lena Kastl, Bruce A Edgar, Wolfgang Wagner, Karsten Gülow, Peter H Krammer

Open access · hybridAbstract read
In one paragraph

Article in FEBS letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  13. In Vivo Effects ofJournal of microbiology and biotechnology · 2023
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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

10 authors at 5 institutions in 2 countries.

Tina OberackerTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Jörg BajoratTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sabine ZiolaTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Anne SchroederTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Daniel RöthTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Lena KastlTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Bruce A EdgarGerman Cancer Research Center (DKFZ), Center for Molecular Biology, University of Heidelberg Alliance, Germany.
Wolfgang WagnerDepartment for Stem Cell Biology and Cellular Engineering, Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University Medical School, Germany.
Karsten GülowTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Peter H KrammerTumor Immunology Program (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany.
German Cancer Research Center · DEHeidelberg University · DEHuntsman Cancer Institute · USRWTH Aachen University · DEUniversity Hospital Regensburg · DE

Funding

DROSOPHILA GENOMICS RESOURCE CENTERP40OD010949 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Andrew Zelhof · 2012 to 2026
$9.4M
NIH HHS P40 OD010949
6 · The paper itself

Abstract

The "free radical theory of aging" suggests that reactive oxygen species (ROS) are responsible for age-related loss of cellular functions and, therefore, represent the main cause of aging. Redox regulation by thioredoxin-1 (TRX) plays a crucial role in responses to oxidative stress. We show that thioredoxin-interacting protein (TXNIP), a negative regulator of TRX, plays a major role in maintaining the redox status and, thereby, influences aging processes. This role of TXNIP is conserved from flies to humans. Age-dependent upregulation of TXNIP results in decreased stress resistance to oxidative challenge in primary human cells and in Drosophila. Experimental overexpression of TXNIP in flies shortens lifespan due to elevated oxidative DNA damage, whereas downregulation of TXNIP enhances oxidative stress resistance and extends lifespan.

Indexed as

AdultAgedAgingAnimalsCarrier ProteinsCell Cycle ProteinsCells, CulturedDNA DamageDrosophila melanogasterHEK293 CellsHumansJurkat CellsLongevityMiddle AgedOxidation-ReductionOxidative StressCarrier ProteinsCell Cycle ProteinsReactive Oxygen SpeciesThioredoxinsTXNIP protein, humanVDUP1 protein, DrosophilaagingDNA damageoxidative stressreactive oxygen speciesthioredoxin

Identifiers

PMID29897613
PMCPMC6099297
OpenAlexW2808561350

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.