ArticleCell reports2025
Homeostatic regulation of nucleoporins is a central driver of nuclear pore biogenesis.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Rapid optogenetic manipulation of autophagy reveals that the nuclear pore complex is a robust autophagy substrate.bioRxiv : the preprint server for biology · 2026Article
- The phenomenon of anhydrobiosis-structural and functional changes in yeast cells.Applied microbiology and biotechnology · 2025Review
- The functional and clinical significance of nucleoporin NUP153 across human cancers: a systematic study based on multi-omics analysis and bench work validation.Frontiers in immunology · 2025Article
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Authors and funding
7 authors.
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Abstract
Nuclear pore complexes (NPCs) are channels that control access to the genome. The number of NPCs that cells assemble varies between different cell types and in disease. However, the mechanisms regulating NPC formation in mammalian cells remain unclear. Using a genome-wide small interfering RNA (siRNA) screen, we identify translation-related factors, proteasome components, and the CCR4-NOT complex as top regulators of NPC assembly and numbers. While inhibition of ribosomal function and protein translation reduces NPC formation, blocking protein degradation or CCR4-NOT function increases NPC numbers. We demonstrate that CCR4-NOT inhibition raises global mRNA levels, increasing the pool of nucleoporin mRNAs available for translation. Upregulation of nucleoporin complexes in CCR4-NOT-inhibited cells allows for higher NPC formation, increasing total NPC numbers in normal and cancer cells. Our findings uncover that nucleoporin mRNA stability and protein homeostasis are major determinants of NPC formation and highlight a role for the CCR4-NOT complex in negatively regulating NPC assembly.
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Registered trials
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