Evidence map›Paper›PMID 25467982›Full record

ArticleNeuron2014

The balance between cytoplasmic and nuclear CaM kinase-1 signaling controls the operating range of noxious heat avoidance.

Lisa C Schild, Laurie Zbinden, Harold W Bell, Yanxun V Yu, Piali Sengupta, Miriam B Goodman, Dominique A Glauser

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

36 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. CaMK modulates sensory neural activity to control longevity and proteostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Molecular Mechanisms Underlying CaInternational journal of molecular sciences · 2022
    Review
  12. The Q-system: A Versatile Repressible Binary Expression System.Methods in molecular biology (Clifton, N.J.) · 2022
    Review
  13. Article
  14. CaeLife · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. HowGenetics · 2019
    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

7 authors at 3 institutions in 2 countries.

Lisa C SchildDepartment of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
Laurie ZbindenDepartment of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
Harold W BellDepartment of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
Yanxun V YuDepartment of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
Piali SenguptaDepartment of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
Miriam B GoodmanDepartment of Molecular and Cellular Physiology, Stanford School of Medicine, Stanford, CA 94305, USA. Electronic address: mbgoodman@stanford.edu.
Dominique A GlauserDepartment of Biology, University of Fribourg, 1700 Fribourg, Switzerland. Electronic address: dominique.glauser@unifr.ch.
Brandeis University · USUniversity of Fribourg · CHStanford Medicine · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Molecular and neuronal mechanisms of thermosensory behaviorR01GM081639 · NIGMS · BRANDEIS UNIVERSITY · PI SENGUPTA, PIALI · 2007 to 2015
$2.6M
Temperature Sensation and Its Behavioral ConsequencesR21NS061147 · NINDS · STANFORD UNIVERSITY · PI GOODMAN, MIRIAM B · 2007 to 2008
$380k
NIGMS NIH HHS R01 GM081639NIH HHS P40 OD010440NINDS NIH HHS R21 NS061147NINDS NIH HHS R21NS061147
6 · The paper itself

Abstract

Through encounters with predators, competitors, and noxious stimuli, animals have evolved defensive responses that minimize injury and are essential for survival. Physiological adaptation modulates the stimulus intensities that trigger such nocifensive behaviors, but the molecular networks that define their operating range are largely unknown. Here, we identify a gain-of-function allele of the cmk-1 CaMKI gene in C. elegans and show that loss of the regulatory domain of the CaMKI enzyme produces thermal analgesia and shifts the operating range for nocifensive heat avoidance to higher temperatures. Such analgesia depends on nuclear CMK-1 signaling, while cytoplasmic CMK-1 signaling lowers the threshold for thermal avoidance. CMK-1 acts downstream of heat detection in thermal receptor neurons and controls neuropeptide release. Our results establish CaMKI as a key regulator of the operating range for nocifensive behaviors and suggest strategies for producing thermal analgesia through the regulation of CaMKI-dependent signaling.

Indexed as

Adaptation, PhysiologicalAnimalsAnimals, Genetically ModifiedAvoidance LearningCaenorhabditis elegansCaenorhabditis elegans ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 1Cell NucleolusCytoplasmEscape ReactionHot TemperatureMutagenesisMutationNeuronsNeuropeptidesNociceptionCaenorhabditis elegans ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 1Neuropeptides

Identifiers

PMID25467982
PMCPMC4318703
OpenAlexW2054063683

What OpenQuestion holds

Textmetadata
LicenceTDM
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.