Evidence map›Paper›PMID 32042051›Full record

ArticleScientific reports2020

SIAH2-mediated and organ-specific restriction of HO-1 expression by a dual mechanism.

Shashipavan Chillappagari, Ratnal Belapurkar, Andreas Möller, Nicole Molenda, Michael Kracht, Susanne Rohrbach, M Lienhard Schmitz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Roots ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
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  16. Regulation of Ferroptosis Pathway by Ubiquitination.Frontiers in cell and developmental biology · 2021
    Review
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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

7 authors at 3 institutions in 2 countries.

Shashipavan ChillappagariInstitute of Biochemistry, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany. shashipavan.chillappagari@innere.med.uni-giessen.de.
Ratnal BelapurkarInstitute of Biochemistry, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany.
Andreas MöllerTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Nicole MolendaDepartment of Physiology, Justus-Liebig-University, D-35392, Giessen, Germany.
Michael KrachtRudolf-Buchheim-Institute of Pharmacology, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany.
Susanne RohrbachDepartment of Physiology, Justus-Liebig-University, D-35392, Giessen, Germany.
M Lienhard SchmitzInstitute of Biochemistry, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany. lienhard.schmitz@biochemie.med.uni-giessen.de.
German Center for Lung Research · DEJustus-Liebig-Universität Gießen · DEQIMR Berghofer Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intracellular levels of the cytoprotective enzyme heme oxygenase-1 (HO-1) are tightly controlled. Here, we reveal a novel mechanism preventing the exaggerated expression of HO-1. The analysis of mice with a knock-out in the ubiquitin E3 ligase seven in absentia homolog 2 (SIAH2) showed elevated HO-1 protein levels in specific organs such as heart, kidney and skeletal muscle. Increased HO-1 protein amounts were also seen in human cells deleted for the SIAH2 gene. The higher HO-1 levels are not only due to an increased protein stability but also to elevated expression of the HO-1 encoding HMOX1 gene, which depends on the transcription factor nuclear factor E2-related factor 2 (NRF2), a known SIAH2 target. Dependent on its RING (really interesting new gene) domain, expression of SIAH2 mediates proteasome-dependent degradation of its interaction partner HO-1. Additionally SIAH2-deficient cells are also characterized by reduced expression levels of glutathione peroxidase 4 (GPX4), rendering the knock-out cells more sensitive to ferroptosis.

Indexed as

AnimalsCRISPR-Cas SystemsDown-RegulationFerroptosisFibroblastsGene Knockdown TechniquesHEK293 CellsHeme Oxygenase-1HumansMembrane ProteinsMiceMice, KnockoutNF-E2-Related Factor 2Nuclear ProteinsOxygenPhospholipid Hydroperoxide Glutathione Peroxidaseglutathione peroxidase 4, mouseHeme Oxygenase-1HMOX1 protein, humanHmox1 protein, mouseMembrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2Nuclear ProteinsOxygenPhospholipid Hydroperoxide Glutathione PeroxidaseProteasome Endopeptidase ComplexSeven in Absentia ProteinsSiah2 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID32042051
PMCPMC7010731
OpenAlexW3004768854

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.