Evidence map›Paper›PMID 26944284›Full record

ReviewMolecular neurobiology2017

A Tale of the Good and Bad: Remodeling of the Microtubule Network in the Brain by Cdk5.

Kavita Shah, Debomoy K Lahiri

Open access · greenAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. 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
  11. Article
  12. Review
  13. Review
  14. CDK5/p35-Dependent Microtubule Reorganization Contributes to Homeostatic Shortening of the Axon Initial Segment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  15. Article
  16. The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022
    Review
  17. Review
  18. Article
  19. Review
  20. Cyclin-dependent kinases and rare developmental disorders.Orphanet journal of rare diseases · 2020
    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

2 authors at 2 institutions in 1 country.

Kavita ShahDepartment of Chemistry and Purdue University Center for Cancer Research, 560 Oval Drive, West Lafayette, IN, 47907, USA. shah23@purdue.edu.
Debomoy K LahiriDepartments of Psychiatry and Medical & Molecular Genetics, Institute of Psychiatric Research, Neuroscience Research Center, Indiana University School of Medicine, 320 W. 15th Street, Indianapolis, IN, 46202-2266, USA.
Indiana University School of MedicinePurdue University West Lafayette · US

Funding

Neurobiological Role of MicroRNA in Alzheimer'sR01AG051086 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2015 to 2019
$1.9M
Exploring FOXO Signaling in Promoting Neurodegeneration in ADR21AG047447 · NIA · PURDUE UNIVERSITY · PI SHAH, KAVITA · 2014 to 2015
$435k
NIA NIH HHS R01 AG051086NIA NIH HHS R21 AG047447
6 · The paper itself

Abstract

Cdk5, a cyclin-dependent kinase family member, is a global orchestrator of neuronal cytoskeletal dynamics. During embryogenesis, Cdk5 is indispensable for brain development. In adults, it is essential for numerous neuronal processes, including higher cognitive functions such as learning and memory formation, drug addiction, pain signaling, and long-term behavior changes through long-term potentiation and long-term depression, all of which rely on rapid alterations in the cytoskeleton. Cdk5 activity becomes deregulated in various brain disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease, attention-deficit hyperactivity disorder, epilepsy, schizophrenia, and ischemic stroke; these all result in profound remodeling of the neuronal cytoskeleton. This Commentary specifically focuses on the pleiotropic contribution of Cdk5 in regulating neuronal microtubule remodeling. Because the vast majority of the physiological substrates of Cdk5 are associated with the neuronal cytoskeleton, our emphasis is on the Cdk5 substrates, such as CRMP2, stathmin, drebrin, dixdc1, axin, MAP2, MAP1B, doublecortin, kinesin-5, and tau, that have allowed to unravel the molecular mechanisms through which Cdk5 exerts its divergent roles in regulating neuronal microtubule dynamics, both in healthy and disease states.

Indexed as

AnimalsBrainCyclin-Dependent Kinase 5CytoskeletonHumansLong-Term PotentiationMicrotubulesNeuronsCDK5 protein, humanCyclin-Dependent Kinase 5Alzheimer diseaseCdk5CytoskeletonMicrotubulesNeurodegenerationp25p35

Identifiers

PMID26944284
PMCPMC5011452
OpenAlexW2292447662

What OpenQuestion holds

Textmetadata
LicenceTDM
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.