Evidence map›Paper›PMID 21253436›Full record

ArticleDrug discovery today. Therapeutic strategies2009

Molecular Roles of Cdk5 in Pain Signaling.

Elias Utreras, Akira Futatsugi, Tej Kumar Pareek, Ashok B Kulkarni

Open access · greenAbstract read
In one paragraph

Article in Drug discovery today. Therapeutic strategies, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Article
  16. Cdk5: An Emerging Kinase in Pain Signaling.Brain disorders & therapy · 2013
    Article
  17. Article
  18. Cdk5 regulates Rap1 activity.Neurochemistry international · 2013
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Elias UtrerasFunctional Genomics Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892.
Akira Futatsugi
Tej Kumar Pareek
Ashok B Kulkarni
National Institutes of Health · USCase Western Reserve University · 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
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

Injury and inflammation trigger activation of several critical cellular pathways in nociceptive signaling in the peripheral nervous system, but their precise molecular mechanisms have not been clearly defined. Cyclin-dependent kinase 5 (Cdk5), a serine/threonine kinase, is mainly expressed in the post-mitotic neurons, and has many important roles in the development, functions and pathophysiology of diseases of the nervous system. Although many functional roles of Cdk5 have been identified in neurons, its precise role in pain signaling has not been well determined. Experimental inflammation in the hind paws of mice resulted in increased mRNA and protein levels of Cdk5 and its activator p35, as well as the Cdk5 activity in nociceptive neurons (Pareek et al., 2006). Furthermore, we also identified that Cdk5 phosphorylates transient receptor potential vanilloid 1 (TRPV1), a key receptor that modulates agonist-induced calcium influx in the neurons (Pareek et al., 2007). We subsequently demonstrated that inflammation triggers increase in Cdk5 activity through activation of early growth response 1 (Egr-1) and p35 expression by tumor necrosis factor alpha (TNF-α) (Utreras et al., 2009). These findings suggest that Cdk5 plays an important role in pain signaling and therefore Cdk5 and its activators are potentially important drug targets for development of novel analgesics to treat neuropathic pain.

Identifiers

PMID21253436
PMCPMC3022326
OpenAlexW2015029595

What OpenQuestion holds

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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.