Evidence map›Paper›PMID 16414974›Full record

ArticleAnnals of the rheumatic diseases2006

Immunoproteasome subunit LMP2 expression is deregulated in Sjogren's syndrome but not in other autoimmune disorders.

S Krause, U Kuckelkorn, T Dörner, G-R Burmester, E Feist, P-M Kloetzel

Open access · greenAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
  5. Article
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  7. Role of Proteasomes in Inflammation.Journal of clinical medicine · 2021
    Review
  8. Article
  9. The ubiquitin proteasome system as a potential therapeutic target for systemic sclerosis.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Potential roles for PA28beta in gastric adenocarcinoma development and diagnosis.Journal of cancer research and clinical oncology · 2010
    Article
  20. Review
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

6 authors at 3 institutions in 2 countries.

S KrauseLaboratory of Molecular Myology, Department of Neurology, Friedrich-Baur-Institute, Ludwig-Maximilians University, Marchioninistrasse 17, 81377 Munich, Germany. sabine.krause@med.uni-muenchen.de
U Kuckelkorn
T Dörner
G-R Burmester
E Feist
P-M Kloetzel
Charité - Universitätsmedizin Berlin · DEInstitute for Transfusion Medicine · USLudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe proteasome system has a pivotal role in the control of the immune response, which suggests that it might be involved in the pathogenesis of autoimmune disorders.

objectiveTo investigate the expression profile of selected proteasomal genes in human peripheral blood mononuclear cells in patients with a variety of autoimmune diseases compared with healthy subjects.

methodsReal time quantitative RT-PCR was used to analyse the mRNA expression pattern of the proteasome activator subunits PA28alpha and PA28beta and of constitutive proteasome and interferon-gamma-inducible immunoproteasome subunits in peripheral blood mononuclear cells. Simultaneously, protein expression of selected proteasome subunits was quantified by immunoblotting.

resultsUnder systemic inflammatory conditions the proteasome subunits LMP2 (beta1i), LMP7 (beta5i), MECL1 (beta2i), and PA28alpha were expressed abundantly at the protein level in the vast majority of systemic autoimmune disorders. However, simultaneous mRNA and protein quantification showed a characteristic proteasome expression signature in primary Sjögren's syndrome. At the transcript level, the interferon-gamma-responsive subunits LMP2 (beta1i), MECL1 (beta2i), and the proteasome activator subunit PA28alpha were markedly up regulated. In contrast, LMP2 (beta1i) deficiency was evident at the protein level, indicating deregulation of proteasome expression in Sjögren's syndrome.

conclusionsThese data provide evidence for a regulatory defect in the proteasome system in human autoimmune disorders, pointing to a unique role for LMP2 (beta1i) in the pathogenesis of primary Sjögren's syndrome.

Indexed as

Down-RegulationAdultAgedAutoimmune DiseasesBiomarkersBlotting, WesternCase-Control StudiesCell Line, TumorCysteine EndopeptidasesFemaleGene ExpressionHumansInterferon-gammaMaleMiddle AgedMuscle ProteinsBiomarkersCysteine EndopeptidasesInterferon-gammaLMP-2 proteinMuscle ProteinsProteasome Endopeptidase ComplexPSMB10 protein, humanPSME1 protein, humanRNA, Messenger

Identifiers

PMID16414974
PMCPMC1798250
OpenAlexW2163732087

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.