Evidence map›Paper›PMID 20937706›Full record

ArticleThe Journal of experimental medicine2010

Cyclin-dependent kinase 5 activity is required for T cell activation and induction of experimental autoimmune encephalomyelitis.

Tej K Pareek, Eric Lam, Xiaojing Zheng, David Askew, Ashok B Kulkarni, Mark R Chance, Alex Y Huang, Kenneth R Cooke, John J Letterio

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

46 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Monocyte Migration Emerges from a Divergent Chemokine Signaling Network.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. CDK5: Insights into its roles in diseases.Molecular biology reports · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022
    Review
  14. Three decades of Cdk5.Journal of biomedical science · 2021
    Review
  15. Article
  16. Article
  17. Deletion ofInternational journal of molecular sciences · 2021
    Article
  18. Article
  19. Review
  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

9 authors at 3 institutions in 1 country.

Tej K PareekDivision of Pediatric Hematology/Oncology, Department of Pediatrics, University Hospitals Case Medical Center and The Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA.
Eric Lam
Xiaojing Zheng
David Askew
Ashok B Kulkarni
Mark R Chance
Alex Y Huang
Kenneth R Cooke
John J Letterio
Case Western Reserve University · USUniversity Hospitals Case Medical Center · USNational Institute of Dental and Craniofacial Research · US

Funding

Molecular Roles of Cdk5 in Neuronal Functions and Pain SignalingZIADE000664 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2025
$20.4M
6 · The paper itself

Abstract

Cyclin-dependent kinase 5 (Cdk5) is a ubiquitously expressed serine/threonine kinase. However, a requirement for Cdk5 has been demonstrated only in postmitotic neurons where there is abundant expression of its activating partners p35 and/or p39. Although hyperactivation of the Cdk5-p35 complex has been found in a variety of inflammatory neurodegenerative disorders, the potential contribution of nonneuronal Cdk5-p35 activity has not been explored in this context. We describe a previously unknown function of the Cdk5-p35 complex in T cells that is required for induction of experimental autoimmune encephalomyelitis (EAE). T cell receptor (TCR) stimulation leads to a rapid induction of Cdk5-p35 expression that is required for T lymphocyte activation. Chimeric mice lacking Cdk5 gene expression in hematopoietic tissues (Cdk5(-/-C)) are resistant to induction of EAE, and adoptive transfer of either Cdk5(-/-C) or p35(-/-) encephalitogenic lymphocytes fails to transfer disease. Moreover, our data reveal a novel mechanism involving Cdk5-mediated phosphorylation of the actin modulator coronin 1a on threonine 418. Cdk5-deficient lymphocytes lack this posttranslational modification of coronin 1a and exhibit defective TCR-induced actin polarization and reduced migration toward CCL-19. These data define a distinct role for Cdk5 in lymphocyte biology and suggest that inhibition of this kinase may be beneficial in the treatment of T cell-mediated inflammatory disorders.

Indexed as

Gene Expression Regulation, EnzymologicLymphocyte ActivationAnimalsCell MovementCyclin-Dependent Kinase 5Encephalomyelitis, Autoimmune, ExperimentalHematopoietic Stem Cell TransplantationMiceMice, KnockoutMicrofilament ProteinsMultiple SclerosisMultiprotein ComplexesReceptors, Antigen, T-CellT-LymphocytesTransplantation ChimeraTransplantation, HomologousCdk5 protein, mousecoronin proteinsCyclin-Dependent Kinase 5Microfilament ProteinsMultiprotein ComplexesReceptors, Antigen, T-Cell

Identifiers

PMID20937706
PMCPMC2964575
OpenAlexW2162704072

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.