Evidence map›Paper›PMID 29453826›Full record

ReviewProteomics2018

Protein Turnover in Aging and Longevity.

Nathan Basisty, Jesse G Meyer, Birgit Schilling

Open access · hybridAbstract readReview
In one paragraph

Review in Proteomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  18. Review
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3 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Nathan BasistyThe Buck Institute for Research on Aging, Novato, CA, USA.ORCID 0000-0001-6173-1139
Jesse G MeyerThe Buck Institute for Research on Aging, Novato, CA, USA.
Birgit SchillingThe Buck Institute for Research on Aging, Novato, CA, USA.
Buck Institute for Research on Aging · US

Funding

Training in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8M
Molecular pathogenesis of skeletal muscle atrophyR01AR071762 · NIAMS · UNIVERSITY OF IOWA · PI ADAMS, CHRISTOPHER M · 2017 to 2021
$2.4M
Molecular Mechanisms of Age-related Muscle LossI01BX000976 · VA · IOWA CITY VA MEDICAL CENTER · PI YOREK, MARK A. · 2012 to 2022
–
BLRD VA I01 BX000976NIAMS NIH HHS R01 AR071762NIA NIH HHS T32 AG000266
6 · The paper itself

Abstract

Progressive loss of proteostasis is a hallmark of aging that is marked by declines in various components of proteostasis machinery, including: autophagy, ubiquitin-mediated degradation, protein synthesis, and others. While declines in proteostasis have historically been observed as changes in these processes, or as bulk changes in the proteome, recent advances in proteomic methodologies have enabled the comprehensive measurement of turnover directly at the level of individual proteins in vivo. These methods, which utilize a combination of stable-isotope labeling, mass spectrometry, and specialized software analysis, have now been applied to various studies of aging and longevity. Here we review the role of proteostasis in aging and longevity, with a focus on the proteomic methods available to conduct protein turnover in aging models and the insights these studies have provided thus far.

Indexed as

AgingLongevityProteostasisAnimalsHumansProteinsProteinsagingmass spectrometryprotein turnoverproteostasisstable isotope labeling

Identifiers

PMID29453826
PMCPMC6022828
OpenAlexW2790315190

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.