Evidence map›Paper›PMID 31042473›Full record

ArticleCell reports2019

Aryl Hydrocarbon Receptor Interacting Protein Maintains Germinal Center B Cells through Suppression of BCL6 Degradation.

Dijue Sun, Urszula Stopka-Farooqui, Sayka Barry, Ezra Aksoy, Gregory Parsonage, Anna Vossenkämper, Melania Capasso, Xinyu Wan, Sherine Norris, Jennifer L Marshall and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. 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
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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Genetics of familial acromegaly and pituitary gigantism.The Journal of clinical endocrinology and metabolism · 2026
    Review
  3. Article
  4. SUMO-specific protease 1 regulates germinal center B cell response through deSUMOylation of PAX5.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Germline Variants in Sporadic Pituitary Adenomas.Journal of the Endocrine Society · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. 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

16 authors at 4 institutions in 1 country.

Dijue SunCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Urszula Stopka-FarooquiCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Sayka BarryEndocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Ezra AksoyCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Gregory ParsonageExperimental Medicine & Rheumatology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Anna VossenkämperCenter for Immunobiology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Melania CapassoBarts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Xinyu WanCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Sherine NorrisCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Jennifer L MarshallInstitute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2TT, UK.
Andrew ClearBarts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
John GribbenBarts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Thomas T MacDonaldCenter for Immunobiology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Christopher D BuckleyInstitute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2TT, UK.
Márta KorbonitsEndocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Oliver HaworthCenter of Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Department of Biological Sciences, Westminster University, London W1W 6UW, UK. Electronic address: o.haworth@westminster.ac.uk.
Queen Mary University of London · GBUniversity of Birmingham · GBWilliam Harvey Research Institute · GBUniversity of Westminster · GB

Funding

Arthritis Research UKMedical Research Council MR/M018539/1Medical Research Council MR/M023230/1Versus Arthritis 19867Wellcome Trust
6 · The paper itself

Abstract

B cell lymphoma-6 (BCL6) is highly expressed in germinal center B cells, but how its expression is maintained is still not completely clear. Aryl hydrocarbon receptor interacting protein (AIP) is a co-chaperone of heat shock protein 90. Deletion of Aip in B cells decreased BCL6 expression, reducing germinal center B cells and diminishing adaptive immune responses. AIP was required for optimal AKT signaling in response to B cell receptor stimulation, and AIP protected BCL6 from ubiquitin-mediated proteasomal degradation by the E3-ubiquitin ligase FBXO11 by binding to the deubiquitinase UCHL1, thus helping to maintain the expression of BCL6. AIP was highly expressed in primary diffuse large B cell lymphomas compared to healthy tissue and other tumors. Our findings describe AIP as a positive regulator of BCL6 expression with implications for the pathobiology of diffuse large B cell lymphoma.

Indexed as

AdultAgedAged, 80 and overAnimalsB-LymphocytesF-Box ProteinsFemaleGerminal CenterHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLymphoma, Large B-Cell, DiffuseMaleMiceMiddle AgedProteasome Endopeptidase Complexaryl hydrocarbon receptor-interacting proteinBCL6 protein, humanF-Box ProteinsFBXO11 protein, humanIntracellular Signaling Peptides and ProteinsProteasome Endopeptidase ComplexProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-bcl-6Ubiquitin ThiolesteraseUCHL1 protein, humanAIPBCL6FBXO11lymphomaubiquitinationUCHL1

Identifiers

PMID31042473
PMCPMC6506688
OpenAlexW2943671120

What OpenQuestion holds

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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.