ArticleThe EMBO journal2007
Opposed growth factor signals control protein degradation in muscles of Caenorhabditis elegans.
Article in The EMBO journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Eldecalcitol prevents muscle loss by suppressing PI3K/AKT/FOXOs pathway in orchiectomized mice.Frontiers in pharmacology · 2022Article
- Triiodothyronine (T3) enhances lifespan and protects against oxidative stress via activation of Klotho in Caenorhabditis elegans.Biogerontology · 2021Article
- Systemic muscle wasting and coordinated tumour response drive tumourigenesis.Nature communications · 2020Article
- Greater loss of mitochondrial function with ageing is associated with earlier onset of sarcopenia inAging · 2018Article
- Functional phosphatome requirement for protein homeostasis, networked mitochondria, and sarcomere structure in C. elegans muscle.Journal of cachexia, sarcopenia and muscle · 2017Article
- FOXO/DAF-16 Activation Slows Down Turnover of the Majority of Proteins in C. elegans.Cell reports · 2016Article
- Degenerin channel activation causes caspase-mediated protein degradation and mitochondrial dysfunction in adult C. elegans muscle.Journal of cachexia, sarcopenia and muscle · 2016Article
- Methods to assess subcellular compartments of muscle in C. elegans.Journal of visualized experiments : JoVE · 2014Article
- Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases.Antioxidants & redox signaling · 2014Article
- Maintenance of muscle myosin levels in adult C. elegans requires both the double bromodomain protein BET-1 and sumoylation.Biology open · 2013Article
- Reduced insulin/insulin-like growth factor-1 signaling and dietary restriction inhibit translation but preserve muscle mass in Caenorhabditis elegans.Molecular & cellular proteomics : MCP · 2013Article
- Knockdown of the C. elegans kinome identifies kinases required for normal protein homeostasis, mitochondrial network structure, and sarcomere structure in muscle.Cell communication and signaling : CCS · 2013Article
- Evaluation of the Fluids Mixing Enclosure System for Life Science Experiments During a CommercialAdvances in space research : the official journal of the Committee on Space Research (COSPAR) · 2013Article
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- Review
- Identification of novel genes involved in sarcopenia through RNAi screening in Caenorhabditis elegans.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Article
- Calpains mediate integrin attachment complex maintenance of adult muscle in Caenorhabditis elegans.PLoS genetics · 2012Article
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- Epidermal growth factor and aging: a signaling molecule reveals a new eye opening function.Aging · 2011Review
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Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to contractile function, muscle provides a metabolic buffer by degrading protein in times of organismal need. Protein is also degraded during adaptive muscle remodeling upon exercise, but extreme degradation in diverse clinical conditions can compromise function(s) and threaten life. Here, we show how two independent signals interact to control protein degradation. In striated muscles of Caenorhabditis elegans, reduction of insulin-like signaling via DAF-2 insulin/IGF receptor or its intramuscular effector PtdIns-3-kinase (PI3K) causes unexpected activation of MAP kinase (MAPK), consequent activation of pre-existing systems for protein degradation, and progressive impairment of mobility. Degradation is prevented by mutations that increase signal downstream of PI3K or by disruption of autocrine signal from fibroblast growth factor (FGF) via the FGF receptor and its effectors in the Ras-MAPK pathway. Thus, the activity of constitutive protein degradation systems in normal muscle is minimized by a balance between directly interacting signaling pathways, implying that physiological, pathological, or therapeutic alteration of this balance may contribute to muscle remodeling or wasting.
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Registered trials
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.