ArticleNature cell biology2024
Nuclear proteasomes buffer cytoplasmic proteins during autophagy compromise.
Article in Nature cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- G3BP1 depletion, observed in Parkinson's Disease, drives Golgi-lysosome-autophagy defects.Cell death and differentiation · 2026Article
- 20S proteasome-regulated proteostasis in ELVAs is critical for oocyte-to-embryo transition and female fertility.The EMBO journal · 2026Article
- Breaking the proteasome balance: α-synuclein and the ubiquitin-proteasome system.Frontiers in cell and developmental biology · 2026Review
- The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss.Frontiers in molecular neuroscience · 2026Article
- FUT3-B3GNT3 interaction promotes pancreatic cancer progression and chemoresistance via NF-κB signaling mediated autophagy.European journal of medical research · 2025Article
- Nuclear basket nucleoporin MoNup50 is essential for fungal development, pathogenicity, and autophagy in Magnaporthe oryzae.Cell communication and signaling : CCS · 2025Article
- Nuclear proteasomes as a backup for autophagy: interconnected proteostasis pathways.Autophagy · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a conserved pathway where cytoplasmic contents are engulfed by autophagosomes, which then fuse with lysosomes enabling their degradation. Mutations in core autophagy genes cause neurological conditions, and autophagy defects are seen in neurodegenerative diseases such as Parkinson's disease and Huntington's disease. Thus, we have sought to understand the cellular pathway perturbations that autophagy-perturbed cells are vulnerable to by seeking negative genetic interactions such as synthetic lethality in autophagy-null human cells using available data from yeast screens. These revealed that loss of proteasome and nuclear pore complex components cause synergistic viability changes akin to synthetic fitness loss in autophagy-null cells. This can be attributed to the cytoplasm-to-nuclear transport of proteins during autophagy deficiency and subsequent degradation of these erstwhile cytoplasmic proteins by nuclear proteasomes. As both autophagy and cytoplasm-to-nuclear transport are defective in Huntington's disease, such cells are more vulnerable to perturbations of proteostasis due to these synthetic interactions.
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Registered trials
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