Evidence map›Paper›PMID 36412904›Full record

ArticleMedical sciences (Basel, Switzerland)2022

Transient Receptor Potential Vanilloid 1 Signaling Is Independent on Protein Kinase A Phosphorylation of Ankyrin-Rich Membrane Spanning Protein.

Antonio Pellegrino, Sandra Mükusch, Viola Seitz, Christoph Stein, Friedrich W Herberg, Harald Seitz

Open access · goldAbstract read
In one paragraph

Article in Medical sciences (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 87% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. 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

6 authors at 4 institutions in 1 country.

Antonio PellegrinoFraunhofer Institute for Cell Therapy and Immunology, 14476 Potsdam, Germany.
Sandra MükuschFraunhofer Institute for Cell Therapy and Immunology, 14476 Potsdam, Germany.
Viola SeitzInstitute of Experimental Anaesthesiology, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany.ORCID 0000-0002-8086-8090
Christoph SteinInstitute of Experimental Anaesthesiology, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany.ORCID 0000-0001-5240-6836
Friedrich W HerbergDepartment of Biochemistry, University of Kassel, 34132 Kassel, Germany.ORCID 0000-0001-7117-7653
Harald SeitzFraunhofer Institute for Cell Therapy and Immunology, 14476 Potsdam, Germany.ORCID 0000-0003-2939-8131
Fraunhofer Institute for Cell Therapy and Immunology · DECharité - Universitätsmedizin Berlin · DEMedizinische Hochschule Brandenburg Theodor Fontane · DEUniversity of Kassel · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sensory ion channel transient receptor potential vanilloid 1 (TRPV1) is mainly expressed in small to medium sized dorsal root ganglion neurons, which are involved in the transfer of acute noxious thermal and chemical stimuli. The Ankyrin-rich membrane spanning protein (ARMS) interaction with TRPV1 is modulated by protein kinase A (PKA) mediating sensitization. Here, we hypothesize that PKA phosphorylation sites of ARMS are crucial for the modulation of TRPV1 function, and that the phosphorylation of ARMS is facilitated by the A-kinase anchoring protein 79 (AKAP79). We used transfected HEK293 cells, immunoprecipitation, calcium flux, and patch clamp experiments to investigate potential PKA phosphorylation sites in ARMS and in ARMS-related peptides. Additionally, experiments were done to discriminate between PKA and protein kinase D (PKD) phosphorylation. We found different interaction ratios for TRPV1 and ARMS mutants lacking PKA phosphorylation sites. The degree of TRPV1 sensitization by ARMS mutants is independent on PKA phosphorylation. AKAP79 was also involved in the TRPV1/ARMS/PKA signaling complex. These data show that ARMS is a PKA substrate via AKAP79 in the TRPV1 signaling complex and that all four proteins interact physically, regulating TRPV1 sensitization in transfected HEK293 cells. To assess the physiological and/or therapeutic significance of these findings, similar investigations need to be performed in native neurons and/or in vivo.

Indexed as

AnkyrinsMembrane ProteinsCyclic AMP-Dependent Protein KinasesHEK293 CellsHumansNerve Tissue ProteinsPhosphorylationTRPV Cation ChannelsAnkyrinsCyclic AMP-Dependent Protein KinasesKIDINS220 protein, humanMembrane ProteinsNerve Tissue ProteinsTRPV1 protein, humanTRPV Cation ChannelsAKAP79ARMSpainphosphorylationPKATRPV1

Identifiers

PMID36412904
PMCPMC9680306
OpenAlexW4309605124

What OpenQuestion holds

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Registered trials

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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.