Evidence map›Paper›PMID 18829898›Full record

ArticleAmerican journal of physiology. Cell physiology2008

Genome-wide RNAi screen and in vivo protein aggregation reporters identify degradation of damaged proteins as an essential hypertonic stress response.

Keith P Choe, Kevin Strange

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

48 citing papers in PubMed, 75 citations in OpenAlex.

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  13. The C. elegans Hypertonic Stress Response: Big Insights from Shrinking Worms.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Review
  14. Automated phenotyping ofMicrosystems & nanoengineering · 2020
    Article
  15. Article
  16. Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective.International journal of molecular sciences · 2019
    Review
  17. 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

2 authors at 1 institution in 1 country.

Keith P ChoeVanderbilt Univ. Medical Center, S. Nashville, TN 37232-2520, USA.
Kevin Strange
Vanderbilt University Medical Center · US

Funding

Regulation of a C. elegans CIC channel by phosphorylation and membrane retrievalR01DK061168 · NIDDK · VANDERBILT UNIVERSITY · PI STRANGE, KEVIN · 2001 to 2013
$4.1M
Identification of GCK-3 signaling pathways in C. elegansF32GM077904 · NIGMS · VANDERBILT UNIVERSITY · PI CHOE, KEITH PATRICK · 2006 to 2008
$120k
NIDDK NIH HHS R01 DK-61168NIGMS NIH HHS F32 GM-077904
6 · The paper itself

Abstract

The damaging effects of hypertonic stress on cellular proteins are poorly defined, and almost nothing is known about the pathways that detect and repair hypertonicity-induced protein damage. To begin addressing these problems, we screened approximately 19,000 Caenorhabditis elegans genes by RNA interference (RNAi) feeding and identified 40 that are essential for survival during acute hypertonic stress. Half (20 of 40) of these genes encode proteins that function to detect, transport, and degrade damaged proteins, including components of the ubiquitin-proteasome system, endosomal sorting complexes, and lysosomes. High-molecular-weight ubiquitin conjugates increase during hypertonic stress, suggesting a global change in the ubiquitinylation state of endogenous proteins. Using a polyglutamine-containing fluorescent reporter, we demonstrate that cell shrinkage induces rapid protein aggregation in vivo and that many of the genes that are essential for survival during hypertonic stress function to prevent accumulation of aggregated proteins. High levels of urea, a strong protein denaturant, do not cause aggregation, suggesting that factors such as macromolecular crowding also contribute to protein aggregate formation during cell shrinkage. Acclimation of C. elegans to mild hypertonicity dramatically increases the osmotic threshold for protein aggregation, demonstrating that protein aggregation-inhibiting pathways are activated by osmotic stress. Our studies demonstrate that hypertonic stress induces protein damage in vivo and that detection and degradation of damaged proteins are essential mechanisms for survival under hypertonic conditions.

Indexed as

RNA InterferenceAnimalsBlotting, WesternCaenorhabditis elegansCaenorhabditis elegans ProteinsGene ExpressionHypertonic SolutionsMicroscopy, ConfocalOsmosisOsmotic PressureStress, PhysiologicalCaenorhabditis elegans ProteinsHypertonic Solutions

Identifiers

PMID18829898
PMCPMC2603564
OpenAlexW2158932513

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.