Evidence map›Paper›PMID 31676602›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Phosphorylation of TRPV1 S801 Contributes to Modality-Specific Hyperalgesia in Mice.

John Joseph, Lintao Qu, Sheng Wang, Martin Kim, Daniel Bennett, Jin Ro, Michael J Caterina, Man-Kyo Chung

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

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  11. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
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  19. Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.bioRxiv : the preprint server for biology · 2023
    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 3 institutions in 1 country.

John JosephDepartment of Neural and Pain Sciences, School of Dentistry, Program in Neuroscience, Center to Advance Chronic Pain Research, The University of Maryland, Baltimore, Maryland 21201.
Lintao QuNeurosurgery Pain Research Institute and Department of Neurosurgery, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and.
Sheng WangDepartment of Neural and Pain Sciences, School of Dentistry, Program in Neuroscience, Center to Advance Chronic Pain Research, The University of Maryland, Baltimore, Maryland 21201.
Martin KimDepartment of Neural and Pain Sciences, School of Dentistry, Program in Neuroscience, Center to Advance Chronic Pain Research, The University of Maryland, Baltimore, Maryland 21201.
Daniel BennettNeurosurgery Pain Research Institute and Department of Neurosurgery, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and.
Jin RoDepartment of Neural and Pain Sciences, School of Dentistry, Program in Neuroscience, Center to Advance Chronic Pain Research, The University of Maryland, Baltimore, Maryland 21201.
Michael J CaterinaNeurosurgery Pain Research Institute and Department of Neurosurgery, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and.
Man-Kyo ChungDepartment of Neural and Pain Sciences, School of Dentistry, Program in Neuroscience, Center to Advance Chronic Pain Research, The University of Maryland, Baltimore, Maryland 21201, mchung@umaryland.edu.
University of Maryland, Baltimore · USJohns Hopkins University · USJohns Hopkins Hospital · US

Funding

Primary afferent plasticity in chronic painR01DE027731 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI CHUNG, MAN-KYO, WEI, FENG · 2018 to 2022
$2.7M
Genetic and post-translational modifications of TRPV1 in craniofacial painR01DE023846 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI CHUNG, MAN-KYO · 2014 to 2018
$1.9M
TRPV1 Modulation during Craniofacial Neuropathy and its Contribution to Chronic PainF31DE027270 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI JOSEPH, JOHN · 2017 to 2018
$77k
NIDCR NIH HHS F31 DE027270NIDCR NIH HHS R01 DE023846NIDCR NIH HHS R01 DE027731
6 · The paper itself

Abstract

Transient receptor potential vanilloid subtype 1 (TRPV1) is a nonselective cationic channel activated by painful stimuli such as capsaicin and noxious heat, and enriched in sensory neurons of the pain pathway. During inflammation, chemical mediators activate protein kinases (such as PKC) that phosphorylate TRPV1 and thereby enhance its function, with consequent increases in nociceptor sensitization. However, the causal relationships between TRPV1 phosphorylation and pathological pain remain unexplored. To directly investigate the roles of one specific TRPV1 phosphorylation event

Indexed as

AnimalsGanglia, SpinalHot TemperatureHyperalgesiaInflammationMiceMice, TransgenicPain MeasurementPhosphorylationPhysical StimulationProtein Kinase CSensory Receptor CellsTRPV Cation ChannelsProtein Kinase CTRPV1 protein, mouseTRPV Cation Channelsinflammationmouse geneticspainphosphorylationprotein kinase CTRPV1

Identifiers

PMID31676602
PMCPMC6978941
OpenAlexW2983603509

What OpenQuestion holds

Textmetadata
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.