Evidence map›Paper›PMID 26399293›Full record

ArticleMolecular biology of the cell2015

Peptide TFP5/TP5 derived from Cdk5 activator P35 provides neuroprotection in the MPTP model of Parkinson's disease.

B K Binukumar, Varsha Shukla, Niranjana D Amin, Philip Grant, M Bhaskar, Susan Skuntz, Joseph Steiner, Harish C Pant

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. A patent review of cyclin-dependent kinase 5 (CDK5) inhibitors (1999-2025).Frontiers in bioengineering and biotechnology · 2026
    Review
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  12. Therapeutic effects of TP5, a Cdk5/p25 inhibitor, inCurrent research in neurobiology · 2021
    Article
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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

8 authors at 1 institution in 1 country.

B K BinukumarNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Varsha ShuklaNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Niranjana D AminNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Philip GrantNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
M BhaskarNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Susan SkuntzNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Joseph SteinerNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Harish C PantNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 panth@ninds.nih.gov.
National Institutes of Health · US

Funding

Cyclin-dependent kinase 5 (Cdk5 physiology and pathology)ZIANS003104 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI PANT, HARISH C · 2009 to 2016
$9.6M
Intramural NIH HHS
6 · The paper itself

Abstract

Parkinson's disease (PD) is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. Recent evidence indicates that cyclin-dependent kinase 5 (Cdk5) is inappropriately activated in several neurodegenerative conditions, including PD. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Previously we reported that TFP5 peptide has neuroprotective effects in animal models of Alzheimer's disease. Here we show that TFP5/TP5 selective inhibition of Cdk5/p25 hyperactivation in vivo and in vitro rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP/MPP+) in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show selective inhibition of Cdk5/p25 -hyperactivation by TFP5/TP5 peptide, which identifies the kinase as a potential therapeutic target to reduce neurodegeneration in Parkinson's disease.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmino Acid SequenceAnimalsCyclin-Dependent Kinase 5Disease Models, AnimalDopamineMaleMiceMice, Inbred C57BLMolecular Sequence DataNerve Tissue ProteinsNeuronsNeuroprotective AgentsParkinson DiseasePeptide FragmentsSubstantia Nigra1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineCyclin-Dependent Kinase 5DopamineNerve Tissue Proteinsneuronal Cdk5 activator (p25-p35)Neuroprotective AgentsPeptide Fragments

Identifiers

PMID26399293
PMCPMC4666141
OpenAlexW2335858257

What OpenQuestion holds

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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.