ArticleScience advances2023
Buffering of genetic dominance by allele-specific protein complex assembly.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- Retinoic Acid Signalling Regulates Zebrafish Tooth Germ Repair Following Injury.Cell proliferation · 2026Article
- Molecular evolution in light of regulatory-coding epistasis.EMBO reports · 2026Review
- Integrating 730,947 exome sequences with clinical literature improves gene discovery.medRxiv : the preprint server for health sciences · 2026Article
- Phenotypic dominance emerges from activity fitness functions and molecular interactions.Genetics · 2026Article
- Prevalence of loss-of-function, gain-of-function and dominant-negative mechanisms across genetic disease phenotypes.Nature communications · 2025Article
- Leveraging protein structural information to improve variant effect prediction.Current opinion in structural biology · 2025Review
- Protein structural context of cancer mutations reveals molecular mechanisms and candidate driver genes.Cell reports · 2024Article
- De novo missense variants in HDAC3 leading to epigenetic machinery dysfunction are associated with a variable neurodevelopmental disorder.American journal of human genetics · 2024Article
- Mutational biases favor complexity increases in protein interaction networks after gene duplication.Molecular systems biology · 2024Article
- Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.Cell & bioscience · 2024Review
- Proteome-scale prediction of molecular mechanisms underlying dominant genetic diseases.PloS one · 2024Article
- Benefits of co-translational complex assembly for cellular fitness.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein complex assembly often occurs while subunits are being translated, resulting in complexes whose subunits were translated from the same mRNA in an allele-specific manner. It has thus been hypothesized that such cotranslational assembly may counter the assembly-mediated dominant-negative effect, whereby co-assembly of mutant and wild-type subunits "poisons" complex activity. Here, we show that cotranslationally assembling subunits are much less likely to be associated with autosomal dominant relative to recessive disorders, and that subunits with dominant-negative disease mutations are significantly depleted in cotranslational assembly compared to those associated with loss-of-function mutations. We also find that complexes with known dominant-negative effects tend to expose their interfaces late during translation, lessening the likelihood of cotranslational assembly. Finally, by combining complex properties with other features, we trained a computational model for predicting proteins likely to be associated with non-loss-of-function disease mechanisms, which we believe will be of considerable utility for protein variant interpretation.
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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.