Evidence map›Paper›PMID 26008897›Full record

ArticleThe Journal of experimental medicine2015

DYRK1A controls the transition from proliferation to quiescence during lymphoid development by destabilizing Cyclin D3.

Benjamin J Thompson, Rahul Bhansali, Lauren Diebold, Daniel E Cook, Lindsay Stolzenburg, Anne-Sophie Casagrande, Thierry Besson, Bertrand Leblond, Laurent Désiré, Sébastien Malinge and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 82 citations in OpenAlex.

  1. Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026
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  12. DYRK1A roles in human neural progenitors.Frontiers in neuroscience · 2025
    Article
  13. Article
  14. Article
  15. Sex specific emergence of trisomicbioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Article
  18. Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024
    Review
  19. Article
  20. 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

11 authors at 3 institutions in 2 countries.

Benjamin J ThompsonDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208.
Rahul BhansaliDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208.
Lauren DieboldDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208.
Daniel E CookDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208.
Lindsay StolzenburgDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208.
Anne-Sophie CasagrandeDiaxonhit, 75013 Paris, France.
Thierry BessonNormandie Université, COBRA, UMR 6014 and FR 3038; Université Rouen; INSA Rouen; Centre National de la Recherche Scientifique, Bâtiment IRCOF, 76821 Mont St. Aignan, France.
Bertrand LeblondDiaxonhit, 75013 Paris, France.
Laurent DésiréDiaxonhit, 75013 Paris, France.
Sébastien MalingeINSERM U985, Gustave Roussy, 94800 Villejuif, France.
John D CrispinoDivision of Hematology/Oncology, Northwestern University, Chicago, IL 60208 j-crispino@northwestern.edu.
Northwestern University · USInserm · FRInstitut National des Sciences Appliquées Rouen Normandie · FR

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Mechanisms of Leukemogenesis in Down SyndromeR01CA101774 · NCI · UNIVERSITY OF CHICAGO · PI CRISPINO, JOHN D · 2003 to 2021
$6.1M
NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA101774
6 · The paper itself

Abstract

Pre-B and pre-T lymphocytes must orchestrate a transition from a highly proliferative state to a quiescent one during development. Cyclin D3 is essential for these cells' proliferation, but little is known about its posttranslational regulation at this stage. Here, we show that the dual specificity tyrosine-regulated kinase 1A (DYRK1A) restrains Cyclin D3 protein levels by phosphorylating T283 to induce its degradation. Loss of DYRK1A activity, via genetic inactivation or pharmacologic inhibition in mice, caused accumulation of Cyclin D3 protein, incomplete repression of E2F-mediated gene transcription, and failure to properly couple cell cycle exit with differentiation. Expression of a nonphosphorylatable Cyclin D3 T283A mutant recapitulated these defects, whereas inhibition of Cyclin D:CDK4/6 mitigated the effects of DYRK1A inhibition or loss. These data uncover a previously unknown role for DYRK1A in lymphopoiesis, and demonstrate how Cyclin D3 protein stability is negatively regulated during exit from the proliferative phases of B and T cell development.

Indexed as

LymphopoiesisAllelesAnimalsB-LymphocytesBone Marrow CellsCell ProliferationCyclin D3Dyrk KinasesE2F Transcription FactorsExonsFemaleFlow CytometryGene LibraryGenotypeHEK293 CellsHumansCcnd3 protein, mouseCyclin D3Dyrk KinasesE2F Transcription FactorsProtein Serine-Threonine KinasesProtein-Tyrosine Kinases

Identifiers

PMID26008897
PMCPMC4451127
OpenAlexW2161848021

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.