ArticleAging cell2019
Gene expression modulation by the linker of nucleoskeleton and cytoskeleton complex contributes to proteostasis.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Aging-associated modulation of UFMylation impairs proteostasis in C. elegans.Nature communications · 2026Article
- Isoflurane aggravates pre-existing proteotoxicity in adult nematodes by suppressing mitochondrial fitness.Scientific reports · 2026Article
- Decreased RYR2 Cluster Size and Abnormal SR CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The aging factor EPS8 induces disease-related protein aggregation through RAC signaling hyperactivation.Nature aging · 2025Article
- A nucleolar mechanism suppresses organismal proteostasis by modulating TGFβ/ERK signalling.Nature cell biology · 2025Article
- Article
- Development of a multifunctional bioreactor to evaluate the promotion effects of cyclic stretching and electrical stimulation on muscle differentiation.Bioengineering & translational medicine · 2024Article
- A short peptide protects from age-onset proteotoxicity.Aging cell · 2023Article
- The ANC-1 (Nesprin-1/2) organelle-anchoring protein functions through mitochondria to polarize axon growth in response to SLT-1.PLoS genetics · 2022Article
- Contribution of senescent and reactive astrocytes on central nervous system inflammaging.Biogerontology · 2022Review
- Organismal Protein Homeostasis Mechanisms.Genetics · 2020Review
- Gene expression modulation by the linker of nucleoskeleton and cytoskeleton complex contributes to proteostasis.Aging cell · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cellular mechanisms that act in concert to maintain protein homeostasis (proteostasis) are vital for organismal functionality and survival. Nevertheless, subsets of aggregation-prone proteins form toxic aggregates (proteotoxicity) that in some cases, underlie the development of neurodegenerative diseases. Proteotoxic aggregates are often deposited in the vicinity of the nucleus, a process that is cytoskeleton-dependent. Accordingly, cytoskeletal dysfunction contributes to pathological hallmarks of various neurodegenerative diseases. Here, we asked whether the linker of nucleoskeleton and cytoskeleton (LINC) complex, which bridges these filaments across the nuclear envelope, is needed for the maintenance of proteostasis. Employing model nematodes, we discovered that knocking down LINC components impairs the ability of the worm to cope with proteotoxicity. Knocking down anc-1, which encodes a key component of the LINC complex, modulates the expression of transcription factors and E3 ubiquitin ligases, thereby affecting the rates of protein ubiquitination and impairing proteasome-mediated protein degradation. Our results establish a link between the LINC complex, protein degradation, and neurodegeneration-associated proteotoxicity.
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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.