Evidence map›Paper›PMID 24314125›Full record

ArticleAging cell2014

Integrin-linked kinase modulates longevity and thermotolerance in C. elegans through neuronal control of HSF-1.

Caroline Kumsta, Tsui-Ting Ching, Mayuko Nishimura, Andrew E Davis, Sara Gelino, Hannah H Catan, Xiaokun Yu, Chu-Chiao Chu, Binnan Ong, Siler H Panowski and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.2field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  6. The Thermal Stress Coping Network of the NematodeInternational journal of molecular sciences · 2022
    Review
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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

14 authors at 3 institutions in 1 country.

Caroline KumstaDevelopment, Aging and Regeneration Program, Sanford-Burnham Medical Research Institute, La Jolla, CA, USA.
Tsui-Ting Ching
Mayuko Nishimura
Andrew E Davis
Sara Gelino
Hannah H Catan
Xiaokun Yu
Chu-Chiao Chu
Binnan Ong
Siler H Panowski
Nathan Baird
Rolf Bodmer
Ao-Lin Hsu
Malene Hansen
Sanford Burnham Prebys Medical Discovery Institute · USUniversity of Michigan–Ann Arbor · USSalk Institute for Biological Studies · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Regulation of the Autophagy Process in Organismal AgingR01AG038664 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Malene Hansen · 2011 to 2026
$6.4M
Regulation of Heat Shock Transcription Factor in Long-lived AnimalsR01AG028516 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HSU, AO-LIN ALLEN · 2008 to 2017
$2.8M
Role of autophagy and lipid metabolism in organismal agingR01AG039756 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HANSEN, MALENE · 2011 to 2015
$1.9M
NIA NIH HHS R01 AG028516NIA NIH HHS R01 AG038664NIA NIH HHS R01 AG039756NIH HHS P40 OD010440
6 · The paper itself

Abstract

Integrin-signaling complexes play important roles in cytoskeletal organization and cell adhesion in many species. Components of the integrin-signaling complex have been linked to aging in both Caenorhabditis elegans and Drosophila melanogaster, but the mechanism underlying this function is unknown. Here, we investigated the role of integrin-linked kinase (ILK), a key component of the integrin-signaling complex, in lifespan determination. We report that genetic reduction of ILK in both C. elegans and Drosophila increased resistance to heat stress, and led to lifespan extension in C. elegans without majorly affecting cytoskeletal integrity. In C. elegans, longevity and thermotolerance induced by ILK depletion was mediated by heat-shock factor-1 (HSF-1), a major transcriptional regulator of the heat-shock response (HSR). Reduction in ILK levels increased hsf-1 transcription and activation, and led to enhanced expression of a subset of genes with roles in the HSR. Moreover, induction of HSR-related genes, longevity and thermotolerance caused by ILK reduction required the thermosensory neurons AFD and interneurons AIY, which are known to play a critical role in the canonical HSR. Notably, ILK was expressed in neighboring neurons, but not in AFD or AIY, implying that ILK reduction initiates cell nonautonomous signaling through thermosensory neurons to elicit a noncanonical HSR. Our results thus identify HSF-1 as a novel effector of the organismal response to reduced ILK levels and show that ILK inhibition regulates HSF-1 in a cell nonautonomous fashion to enhance stress resistance and lifespan in C. elegans.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsHeat-Shock ResponseLongevityProtein Serine-Threonine KinasesScaffold Protein ILKSignal TransductionTranscription FactorsCaenorhabditis elegans Proteinsheat shock factor-1, C elegansProtein Serine-Threonine KinasesScaffold Protein ILKTranscription FactorsagingC. elegansheat-shock responseHSF-1integrin signalingPAT-4/ILK

Identifiers

PMID24314125
PMCPMC4059541
OpenAlexW2068090207

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.