Evidence map›Paper›PMID 28963798›Full record

ArticleFEBS letters2017

TRiC/CCT chaperonins are essential for maintaining myofibril organization, cardiac physiological rhythm, and lifespan.

Girish C Melkani, Shruti Bhide, Andrew Han, Jay Vyas, Catherine Livelo, Rolf Bodmer, Sanford I Bernstein

Open access · bronzeAbstract readLetter
In one paragraph

Article in FEBS letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Sorbitol andmicroPublication biology · 2021
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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 2 institutions in 1 country.

Girish C MelkaniDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.ORCID 0000-0003-0353-4633
Shruti BhideDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.
Andrew HanDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.
Jay VyasDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.
Catherine LiveloDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.
Rolf BodmerDevelopment, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.
Sanford I BernsteinDepartment of Biology, Molecular Biology and Heart Institutes, San Diego State University, CA, USA.
San Diego State University · USSanford Burnham Prebys Medical Discovery Institute · US

Funding

Strucutre of the UNC-45 Chaperone and its Interaction with Skeletal Muscle MyosinR01AR055958 · NIAMS · SAN DIEGO STATE UNIVERSITY · PI BERNSTEIN, SANFORD I · 2008 to 2017
$2.5M
Metabolome-Genome Associations for Determining Mechanisms of Aging in DrosophilaR01AG049494 · NIA · UNIVERSITY OF WASHINGTON · PI PROMISLOW, DANIEL EDWARD · 2015 to 2019
$1.8M
Genetic analysis and regulation of laminopathy induced cardiac defectsR21AG049454 · NIA · SAN DIEGO STATE UNIVERSITY · PI MELKANI, GIRISH C. · 2015 to 2016
$469k
Using metabolomics to identify mechanisms of natural variation in agingR56AG049494 · NIA · UNIVERSITY OF WASHINGTON · PI PROMISLOW, DANIEL EDWARD, VILLEN, JUDIT · 2022 to 2022
$319k
NIAMS NIH HHS R01 AR055958NIA NIH HHS R01 AG049494NIA NIH HHS R21 AG049454NIA NIH HHS R56 AG049494
6 · The paper itself

Abstract

We recently reported that CCT chaperonin subunits are upregulated in a cardiac-specific manner under time-restricted feeding (TRF) [Gill S et al. (2015) Science 347, 1265-1269], suggesting that TRiC/CCT has a heart-specific function. To understand the CCT chaperonin function in cardiomyocytes, we performed its cardiac-specific knock-down in the Drosophila melanogaster model. This resulted in disorganization of cardiac actin- and myosin-containing myofibrils and severe physiological dysfunction, including restricted heart diameters, elevated cardiac dysrhythmia and compromised cardiac performance. We also noted that cardiac-specific knock-down of CCT chaperonin significantly shortens lifespans. Additionally, disruption of circadian rhythm yields further deterioration of cardiac function of hypomorphic CCT mutants. Our analysis reveals that both the orchestration of protein folding and circadian rhythms mediated by CCT chaperonin are critical for maintaining heart contractility.

Indexed as

AnimalsChaperoninsCircadian RhythmDrosophila melanogasterDrosophila ProteinsGene Knockdown TechniquesLongevityMyocytes, CardiacMyofibrilsChaperoninsDrosophila Proteinscardiomyopathycircadian clockcytoskeletal proteinsDrosophila geneticsprotein folding and misfoldingTRiC:TCP-1 ring complex chaperonin

Identifiers

PMID28963798
PMCPMC5683924
OpenAlexW2759927322

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.