ArticleMolecular cell2025
Divergent proteome tolerance against gain and loss of chromosome arms.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Deep visual multi-omics profiling links morphology and molecular programs in clear cell renal cell carcinoma.EMBO molecular medicine · 2026Article
- Complex assembly and activity states as multifaceted protein attributes explaining phenotypic variability.Molecular systems biology · 2026Article
- Aneuploidy sensitizes cells to SREBP-pathway inhibition in squamous cell carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Paired CRISPR screens identify mitochondrial metabolism and UBE2H as aneuploid-specific dependencies in human cancer cell lines.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
How aneuploid cells tolerate chromosome arm gains or losses remains an open question. Using an isogenic human lung cell model with either chromosome 3p loss or 3q gain, combined with quantitative mass spectrometry and isotopic labeling, we reveal distinct proteostasis mechanisms for gain- and loss-type aneuploidy. Surprisingly, while compensation for 3q gain is primarily driven by increased degradation of excess protein complex subunits, 3p loss is neither counteracted by global protein degradation nor selectively reduced degradation. Rather, there is a relative upregulation in protein synthesis of those 3p-encoded proteins that participate in stable protein complexes to maintain functional complex stoichiometry. Additionally, 3p-encoded proteins that are in a complex show increased thermal stability in loss-type aneuploidy, potentially via their interactions with other proteins from euploid chromosomes. Together, our findings uncover distinct proteomic buffering strategies that enable cells to tolerate either excessive or deficient single-arm aneuploidy.
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