Evidence map›Paper›PMID 24879856›Full record

ReviewJournal of cell science2014

Cdk5 activity in the brain - multiple paths of regulation.

Kavita Shah, Debomoy K Lahiri

Abstract readReview
In one paragraph

Review in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Neuron-specific epigenetic repression ofbioRxiv : the preprint server for biology · 2026
    Article
  5. Protein kinases as therapeutic targets in Alzheimer's disease: challenges, insights, and new frontiers.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  6. Review
  7. Alzheimer's disease prevention by flavonols and their analogs.The journal of prevention of Alzheimer's disease · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. bioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Article
  14. Role of Glutamate Receptor-related Biomarkers in the Etiopathogenesis of ADHD.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024
    Article
  15. Review
  16. Molecular Changes Associated with Suicide.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. Review

49 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Kavita ShahDepartment of Chemistry, 560 Oval Drive, West Lafayette, IN 47907, USA shah23@purdue.edu.
Debomoy K LahiriLaboratory of Molecular Neurogenetics, Departments of Psychiatry and of Medical & Molecular Genetics, Indiana University School of Medicine, Institute of Psychiatric Research, Neuroscience Research Building, 320 W. 15th St., Indianapolis, IN 46202, USA shah23@purdue.edu.
Indiana University – Purdue University Indianapolis · USPurdue University West Lafayette · US

Funding

Exploring FOXO Signaling in Promoting Neurodegeneration in ADR21AG047447 · NIA · PURDUE UNIVERSITY · PI SHAH, KAVITA · 2014 to 2015
$435k
NIA NIH HHS R21 AG047447
6 · The paper itself

Abstract

Cyclin dependent kinase-5 (Cdk5), a family member of the cyclin-dependent kinases, plays a pivotal role in the central nervous system. During embryogenesis, Cdk5 is indispensable for brain development and, in the adult brain, it is essential for numerous neuronal processes, including higher cognitive functions such as learning and memory formation. However, Cdk5 activity becomes deregulated in several neurological disorders, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, which leads to neurotoxicity. Therefore, precise control over Cdk5 activity is essential for its physiological functions. This Commentary covers the various mechanisms of Cdk5 regulation, including several recently identified protein activators and inhibitors of Cdk5 that control its activity in normal and diseased brains. We also discuss the autoregulatory activity of Cdk5 and its regulation at the transcriptional, post-transcriptional and post-translational levels. We finally highlight physiological and pathological roles of Cdk5 in the brain. Specific modulation of these protein regulators is expected to provide alternative strategies for the development of effective therapeutic interventions that are triggered by deregulation of Cdk5.

Indexed as

Gene Expression RegulationProtein Processing, Post-TranslationalRNA InterferenceAnimalsCognitionCyclin-Dependent Kinase 5Fetal DevelopmentHomeostasisHumansMemoryMolecular Targeted TherapyNeurodegenerative DiseasesCyclin-Dependent Kinase 5Alzheimer’s diseaseAxonal growthCdkCdk5CyclinsExcitotoxicityLearning and memoryNeurodegenerationNeuronal migrationp25p35Pain signallingSynaptic plasticitySynaptogenesisβ-Amyloid

Identifiers

PMID24879856
PMCPMC4038939
OpenAlexW1969417329

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.