Evidence map›Paper›PMID 24359609›Full record

ArticleMolecular pain2013

Activation of cyclin-dependent kinase 5 mediates orofacial mechanical hyperalgesia.

Michaela Prochazkova, Anita Terse, Niranjana D Amin, Bradford Hall, Elias Utreras, Harish C Pant, Ashok B Kulkarni

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. FOXD3-mediated transactivation of ALKBH5 promotes neuropathic pain via mProceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 3 institutions in 2 countries.

Michaela Prochazkova
Anita Terse
Niranjana D Amin
Bradford Hall
Elias Utreras
Harish C Pant
Ashok B KulkarniFunctional Genomics Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. ak40m@nih.gov.
National Institutes of Health · USNational Institute of Dental and Craniofacial Research · USNational Institute of Neurological Disorders and Stroke · 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
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
PHOSPHORYLATION OF NEURONAL CYTOSKELETON IN NEURODEGENERATIVE DISEASESZ01DE000664 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK B. · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 DE000664
6 · The paper itself

Abstract

backgroundCyclin-dependent kinase 5 (Cdk5) is a unique member of the serine/threonine kinase family. This kinase plays an important role in neuronal development, and deregulation of its activity leads to neurodegenerative disorders. Cdk5 also serves an important function in the regulation of nociceptive signaling. Our previous studies revealed that the expression of Cdk5 and its activator, p35, is upregulated in nociceptive neurons during peripheral inflammation. The aim of the present study was to characterize the involvement of Cdk5 in orofacial pain. Since mechanical hyperalgesia is the distinctive sign of many orofacial pain conditions, we adapted an existing orofacial stimulation test to assess the behavioral responses to mechanical stimulation in the trigeminal region of the transgenic mice with either reduced or increased Cdk5 activity.

resultsMice overexpressing or lacking p35, an activator of Cdk5, showed altered phenotype in response to noxious mechanical stimulation in the trigeminal area. Mice with increased Cdk5 activity displayed aversive behavior to mechanical stimulation as indicated by a significant decrease in reward licking events and licking time. The number of reward licking/facial contact events was significantly decreased in these mice as the mechanical intensity increased. By contrast, mice deficient in Cdk5 activity displayed mechanical hypoalgesia.

conclusionsCollectively, our findings demonstrate for the first time the important role of Cdk5 in orofacial mechanical nociception. Modulation of Cdk5 activity in primary sensory neurons makes it an attractive potential target for the development of novel analgesics that could be used to treat multiple orofacial pain conditions.

Indexed as

AnimalsCyclin-Dependent Kinase 5Facial PainHyperalgesiaMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsSignal TransductionTrigeminal GanglionCyclin-Dependent Kinase 5Nerve Tissue Proteinsneuronal Cdk5 activator (p25-p35)

Identifiers

PMID24359609
PMCPMC3882292
OpenAlexW2101360931

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.