Evidence map›Paper›PMID 24009518›Full record

ArticlePLoS genetics2013

Neuronal reprograming of protein homeostasis by calcium-dependent regulation of the heat shock response.

M Catarina Silva, Margarida D Amaral, Richard I Morimoto

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Protein Aggregation in the Pathogenesis of Ischemic Stroke.Cellular and molecular neurobiology · 2021
    Review
  10. Article
  11. Article
  12. Cell-Nonautonomous Regulation of Proteostasis in Aging and Disease.Cold Spring Harbor perspectives in biology · 2020
    Review
  13. Methods to Determine the Role of Autophagy Proteins in C. elegans Aging.Methods in molecular biology (Clifton, N.J.) · 2019
    Article
  14. Article
  15. Cellular clearance of circulating transthyretin decreases cell-nonautonomous proteotoxicity inProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

M Catarina SilvaDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois, United States of America.
Margarida D Amaral
Richard I Morimoto
Rice Institute · USNational Institute of Health Dr. Ricardo Jorge · PT

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
C. elegans Model for Neurodegenerative Diseases of AgingR37AG026647 · NIA · NORTHWESTERN UNIVERSITY · PI MORIMOTO, RICHARD I · 2010 to 2019
$3.9M
C. Elegans Model for Neurodegenerative Diseases of AgingR01AG026647 · NIA · NORTHWESTERN UNIVERSITY · PI MORIMOTO, RICHARD I · 2005 to 2009
$2.0M
NCI NIH HHS P30 CA060553NIA NIH HHS R01 AG026647NIA NIH HHS R37 AG026647
6 · The paper itself

Abstract

Protein quality control requires constant surveillance to prevent misfolding, aggregation, and loss of cellular function. There is increasing evidence in metazoans that communication between cells has an important role to ensure organismal health and to prevent stressed cells and tissues from compromising lifespan. Here, we show in C. elegans that a moderate increase in physiological cholinergic signaling at the neuromuscular junction (NMJ) induces the calcium (Ca(2+))-dependent activation of HSF-1 in post-synaptic muscle cells, resulting in suppression of protein misfolding. This protective effect on muscle cell protein homeostasis was identified in an unbiased genome-wide screening for modifiers of protein aggregation, and is triggered by downregulation of gei-11, a Myb-family factor and proposed regulator of the L-type acetylcholine receptor (AChR). This, in-turn, activates the voltage-gated Ca(2+) channel, EGL-19, and the sarcoplasmic reticulum ryanodine receptor in response to acetylcholine signaling. The release of calcium into the cytoplasm of muscle cells activates Ca(2+)-dependent kinases and induces HSF-1-dependent expression of cytoplasmic chaperones, which suppress misfolding of metastable proteins and stabilize the folding environment of muscle cells. This demonstrates that the heat shock response (HSR) can be activated in muscle cells by neuronal signaling across the NMJ to protect proteome health.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCalciumCalmodulinHeat-Shock ResponseHomeostasisHumansMolecular ChaperonesMuscle CellsNeuromuscular JunctionNeuronsReceptors, CholinergicSignal TransductionTranscription FactorsCaenorhabditis elegans ProteinsCalciumCalmodulinheat shock factor-1, C elegansMolecular ChaperonesReceptors, CholinergicTranscription Factors

Identifiers

PMID24009518
PMCPMC3757039
OpenAlexW2078053139

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.