Evidence map›Paper›PMID 26843529›Full record

ArticleChemical senses2016

Naturally Produced Defensive Alkenal Compounds Activate TRPA1.

Nathaniel T Blair, Benjamin I Philipson, Paige M Richards, Julia F Doerner, Abraham Segura, Wayne L Silver, David E Clapham

Open access · bronzeAbstract read
In one paragraph

Article in Chemical senses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

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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

7 authors at 6 institutions in 1 country.

Nathaniel T BlairHoward Hughes Medical Institute (HHMI), Boston, MA, USA, Department of Cardiology, Boston Children's Hospital, Boston, MA 02115, USA, Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Benjamin I PhilipsonHarvard College, Cambridge, MA 02138, USA.
Paige M RichardsDepartment of Biology, Wake Forest University, Winston-Salem, NC 27106, USA and.
Julia F DoernerHoward Hughes Medical Institute (HHMI), Boston, MA, USA, Department of Cardiology, Boston Children's Hospital, Boston, MA 02115, USA, Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Abraham SeguraWashington University School of Medicine, St. Louis, MO 63110, USA.
Wayne L SilverDepartment of Biology, Wake Forest University, Winston-Salem, NC 27106, USA and.
David E ClaphamHoward Hughes Medical Institute (HHMI), Boston, MA, USA, Department of Cardiology, Boston Children's Hospital, Boston, MA 02115, USA, Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA, dclapham@enders.tch.harvard.edu.
Wake Forest University · USBoston Children's Hospital · USHarvard College Observatory · USHarvard University · USHoward Hughes Medical Institute · USWashington University in St. Louis · US

Funding

TRP Channel Mediated Pain CircuitryP01NS072040 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI WOOLF, CLIFFORD J · 2011 to 2015
$6.7M
NINDS NIH HHS P01 NS072040
6 · The paper itself

Abstract

(E)-2-alkenals are aldehydes containing an unsaturated bond between the alpha and beta carbons. 2-alkenals are produced by many organisms for defense against predators and secretions containing (E)-2-alkenals cause predators to stop attacking and allow the prey to escape. Chemical ecologists have described many alkenal compounds with 3-20 carbons common, having varied positions of double bonds and substitutions. How do these defensive alkenals act to deter predators? We have tested the effects of (E)-2-alkenals with 6-12 carbons on transient receptor potential channels (TRP) commonly found in sensory neurons. We find that (E)-2-alkenals activate transient receptor potential ankyrin subtype 1 (TRPA1) at low concentrations-EC50s 10-100 µM (in 0 added Ca(2+) external solutions). Other TRP channels were either weakly activated (TRPV1, TRPV3) or insensitive (TRPV2, TRPV4, TRPM8). (E)-2-alkenals may activate TRPA1 by modifying cysteine side chains. However, target cysteines include others beyond the 3 in the amino-terminus implicated in activation, as a channel with cysteines at 621, 641, 665 mutated to serine responded robustly. Related chemicals, including the aldehydes hexanal and decanal, and (E)-2-hexen-1-ol also activated TRPA1, but with weaker potency. Rat trigeminal nerve recordings and behavioral experiments showed (E)-2-hexenal was aversive. Our results suggest that TRPA1 is likely a major target of these commonly used defensive chemicals.

Indexed as

Action PotentialsAldehydesAnimalsCalciumCalcium ChannelsCysteineHabituation, PsychophysiologicHEK293 CellsHexanolsHumansMaleMicroscopy, FluorescenceNerve Tissue ProteinsPatch-Clamp TechniquesRatsRats, Sprague-Dawley2-hexanol2-hexenalAldehydesCalciumCalcium ChannelsCysteineHexanolsNerve Tissue ProteinsTransient Receptor Potential ChannelsTRPA1 Cation ChannelTRPA1 protein, humanallomonechemoreceptiondeterrentnociceptortrigeminal sensation

Identifiers

PMID26843529
PMCPMC5863776
OpenAlexW2337301812

What OpenQuestion holds

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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.