Evidence map›Paper›PMID 24612480›Full record

ArticleMolecular pain2014

Alleviation of behavioral hypersensitivity in mouse models of inflammatory pain with two structurally different casein kinase 1 (CK1) inhibitors.

Takashi Kurihara, Eri Sakurai, Masayasu Toyomoto, Isao Kii, Daisuke Kawamoto, Toshihide Asada, Tsutomu Tanabe, Megumu Yoshimura, Masatoshi Hagiwara, Atsuro Miyata

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. 5-HTThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  6. Casein kinase 1α: biological mechanisms and theranostic potential.Cell communication and signaling : CCS · 2018
    Review
  7. Orai1 Plays a Crucial Role in Central Sensitization by Modulating Neuronal Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  8. Article
  9. Article
  10. Casein kinase signaling in axon regeneration.Neural regeneration research · 2016
    Article
  11. Article
  12. Article
  13. 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

10 authors at 4 institutions in 1 country.

Takashi KuriharaDepartment of Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima City, Kagoshima 890-8544, Japan. tkmphm10@m.kufm.kagoshima-u.ac.jp.
Eri Sakurai
Masayasu Toyomoto
Isao Kii
Daisuke Kawamoto
Toshihide Asada
Tsutomu Tanabe
Megumu Yoshimura
Masatoshi Hagiwara
Atsuro Miyata
Kagoshima University · JPKyoto University · JPTokyo Medical and Dental University · JPKumamoto Health Science University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe phylogenetically highly conserved CK1 protein kinases consisting of at least seven isoforms form a distinct family within the eukaryotic protein kinases. CK1 family members play crucial roles in a wide range of signaling activities. However, the functional role of CK1 in somatosensory pain signaling has not yet been fully understood. The aim of this study was to clarify the role of CK1 in the regulation of inflammatory pain in mouse carrageenan and complete Freund's adjuvant (CFA) models.

resultsWe have used two structurally different CK1 inhibitors, TG003 and IC261. TG003, which was originally identified as a cdc2-like kinase inhibitor, had potent inhibitory effects on CK1 isoforms in vitro and in cultured cells. Intrathecal injection of either TG003 (1-100 pmol) or IC261 (0.1-1 nmol) dose-dependently decreased mechanical allodynia and thermal hyperalgesia induced by carrageenan or CFA. Bath-application of either TG003 (1 μM) or IC261 (1 μM) had only marginal effects on spontaneous excitatory postsynaptic currents (sEPSCs) recorded in the substantia gelatinosa neurons of control mice. However, both compounds decreased the frequency of sEPSCs in both inflammatory pain models.

conclusionsThese results suggest that CK1 plays an important pathophysiological role in spinal inflammatory pain transmission, and that inhibition of the CK1 activity may provide a novel strategy for the treatment of inflammatory pain.

Indexed as

AnimalsCarrageenanCasein Kinase ICells, CulturedDisease Models, AnimalEnzyme InhibitorsExcitatory Postsynaptic PotentialsHumansHyperalgesiaIndolesInflammationMaleMembrane PotentialsMiceMice, Inbred C57BLPainCarrageenanCasein Kinase IEnzyme InhibitorsIC 261IndolesPhloroglucinolTG 003Thiazoles

Identifiers

PMID24612480
PMCPMC4008364
OpenAlexW2120855549

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.