Evidence map›Paper›PMID 29587401›Full record

ArticleInternational journal of molecular sciences2018

Inactivation of SREBP-1a Phosphorylation Prevents Fatty Liver Disease in Mice: Identification of Related Signaling Pathways by Gene Expression Profiles in Liver and Proteomes of Peroxisomes.

Birgit Knebel, Sonja Hartwig, Sylvia Jacob, Ulrike Kettel, Martina Schiller, Waltraud Passlack, Cornelia Koellmer, Stefan Lehr, Dirk Müller-Wieland, Jorg Kotzka

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Lipid Metabolism and Cancer.Life (Basel, Switzerland) · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Fatty Liver Due to IncreasedFrontiers in cell and developmental biology · 2019
    Article
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 2 institutions in 1 country.

Birgit KnebelInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. bknebel@ddz.uni-duesseldorf.de.ORCID 0000-0002-5575-4315
Sonja HartwigInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. sonja.hartwig@ddz.uni-duesseldorf.de.
Sylvia JacobInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Sylvia.Jacob@ddz.uni-duesseldorf.de.
Ulrike KettelInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Ulrike.Kettel@ddz.uni-duesseldorf.de.
Martina SchillerInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Martina.Schiller@ddz.uni-duesseldorf.de.
Waltraud PasslackInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Waltraud.Passlack@ddz.uni-duesseldorf.de.
Cornelia KoellmerInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Cornelia.Koellmer@ddz.uni-duesseldorf.de.
Stefan LehrInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. Stefan.Lehr@ddz.uni-duesseldorf.de.
Dirk Müller-WielandClinical Research Centre, Department of Internal Medicine I, University Hospital Aachen, 52074 Aachen, Germany. dirmueller@ukaachen.de.
Jorg KotzkaInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225 Duesseldorf, Germany. joerg.kotzka@ddz.uni-duesseldorf.de.ORCID 0000-0003-1173-9372
Deutsches Diabetes-Zentrum e.V. · DEUniversitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The key lipid metabolism transcription factor sterol regulatory element-binding protein (SREBP)-1a integrates gene regulatory effects of hormones, cytokines, nutrition and metabolites as lipids, glucose, or cholesterol via phosphorylation by different mitogen activated protein kinase (MAPK) cascades. We have previously reported the impact of SREBP-1a phosphorylation on the phenotype in transgenic mouse models with liver-specific overexpression of the N-terminal transcriptional active domain of SREBP-1a (alb-SREBP-1a) or a MAPK phosphorylation site-deficient variant (alb-SREBP-1a∆P; (S63A, S117A, T426V)), respectively. In this report, we investigated the molecular basis of the systemic observations by holistic analyses of gene expression in liver and of proteome patterns in lipid-degrading organelles involved in the pathogenesis of metabolic syndrome, i.e., peroxisomes, using 2D-DIGE and mass spectrometry. The differences in hepatic gene expression and peroxisomal protein patterns were surprisingly small between the control and alb-SREBP-1a mice, although the latter develop a severe phenotype with visceral obesity and fatty liver. In contrast, phosphorylation site-deficient alb-SREBP-1a∆P mice, which are protected from fatty liver disease, showed marked differences in hepatic gene expression and peroxisomal proteome patterns. Further knowledge-based analyses revealed that disruption of SREBP-1a phosphorylation resulted in massive alteration of cellular processes, including signs for loss of targeting lipid pathways.

Indexed as

Disease Models, AnimalMiceAnimalsFatty LiverGene DeletionHumansMaleMetabolic SyndromeMice, Inbred C57BLMice, TransgenicObesity, AbdominalPeroxisomesPhosphorylationProteomeSterol Regulatory Element Binding Protein 1TranscriptomeProteomeSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1fatty liverhepatic gene expressionliver peroxisomesmetabolic syndromeolfactory receptorsperoxisome proteomephosphorylation in lipid metabolismphosphorylation of SREBP-1a

Identifiers

PMID29587401
PMCPMC5979561
OpenAlexW2793506554

What OpenQuestion holds

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Registered trials

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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.