Evidence map›Paper›PMID 31277262›Full record

ArticleInternational journal of molecular sciences2019

Carboplatin Enhances the Activity of Human Transient Receptor Potential Ankyrin 1 through the Cyclic AMP-Protein Kinase A-A-Kinase Anchoring Protein (AKAP) Pathways.

Kanako Miyano, Seiji Shiraishi, Koichiro Minami, Yuka Sudo, Masami Suzuki, Toru Yokoyama, Kiyoshi Terawaki, Miki Nonaka, Hiroaki Murata, Yoshikazu Higami and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Determining 5HTFrontiers in neuroscience · 2021
    Article
  9. Phospho-Mimetic Mutation at Ser602 Inactivates Human TRPA1 Channel.International journal of molecular sciences · 2020
    Article
  10. Article
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

11 authors at 3 institutions in 1 country.

Kanako MiyanoDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Seiji ShiraishiDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Koichiro MinamiDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Yuka SudoDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Masami SuzukiDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Toru YokoyamaDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Kiyoshi TerawakiDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Miki NonakaDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan.
Hiroaki MurataDepartment of Anesthesiology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Yoshikazu HigamiLaboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.ORCID 0000-0003-1381-0777
Yasuhito UezonoDivision of Cancer Pathophysiology, National Cancer Research Institute, Tokyo 104-0045, Japan. yuezono@ncc.go.jp.ORCID 0000-0003-1208-1453
Jichi Medical University · JPNagasaki University · JPTokyo University of Science · JP

Funding

Japan Society for the Promotion of Science 15K08215Japan Society for the Promotion of Science 15K10522Japan Society for the Promotion of Science 16K08568Japan Society for the Promotion of Science 18K08858Japan Society for the Promotion of Science 23790315Japan Society for the Promotion of Science 25860199The Nakatomi Foundation none
6 · The paper itself

Abstract

Carboplatin, an anticancer drug, often causes chemotherapy-induced peripheral neuropathy (PN). Transient receptor potential ankyrin 1 (TRPA1), a non-selective cation channel, is a polymodal nociceptor expressed in sensory neurons. TRPA1 is not only involved in pain transmission, but also in allodynia or hyperalgesia development. However, the effects of TRPA1 on carboplatin-induced PN is unclear. We revealed that carboplatin induced mechanical allodynia and cold hyperalgesia, and the pains observed in carboplatin-induced PN models were significantly suppressed by the TRPA1 antagonist HC-030031 without a change in the level of TRPA1 protein. In cells expressing human TRPA, carboplatin had no effects on changes in intracellular Ca

Indexed as

Signal TransductionA Kinase Anchor ProteinsAnimalsCarboplatinCyclic AMPCyclic AMP-Dependent Protein KinasesHumansHyperalgesiaMaleMiceMice, Inbred C57BLTRPA1 Cation ChannelA Kinase Anchor ProteinsCarboplatinCyclic AMPCyclic AMP-Dependent Protein KinasesTRPA1 Cation ChannelAKAPcAMPcarboplatinCIPNPKATRPA1

Identifiers

PMID31277262
PMCPMC6651390
OpenAlexW2951586037

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.