ArticleJournal of cell science2021
Genome-wide imaging screen uncovers molecular determinants of arsenite-induced protein aggregation and toxicity.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Arsenic binds to nuclear transport factors and disrupts nucleocytoplasmic transport.Journal of cell science · 2025Article
- Direct binding of arsenicals to nuclear transport factors disrupts nucleocytoplasmic transport.bioRxiv : the preprint server for biology · 2025Article
- Membrane transporters modulating the toxicity of arsenic, cadmium, and mercury in human cells.Life science alliance · 2025Article
- Multilevel Regulation of Membrane Proteins in Response to Metal and Metalloid Stress: A Lesson from Yeast.International journal of molecular sciences · 2024Review
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Identification of novel arsenic resistance genes in yeast.MicrobiologyOpen · 2022Article
- Etp1 confers arsenite resistance by affecting ACR3 expression.FEMS yeast research · 2022Article
- Effects of the Toxic Metals Arsenite and Cadmium on α-Synuclein Aggregation In Vitro and in Cells.International journal of molecular sciences · 2021Article
- Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The toxic metalloid arsenic causes widespread misfolding and aggregation of cellular proteins. How these protein aggregates are formed in vivo, the mechanisms by which they affect cells and how cells prevent their accumulation is not fully understood. To find components involved in these processes, we performed a genome-wide imaging screen and identified Saccharomyces cerevisiae deletion mutants with either enhanced or reduced protein aggregation levels during arsenite exposure. We show that many of the identified factors are crucial to safeguard protein homeostasis (proteostasis) and to protect cells against arsenite toxicity. The hits were enriched for various functions including protein biosynthesis and transcription, and dedicated follow-up experiments highlight the importance of accurate transcriptional and translational control for mitigating protein aggregation and toxicity during arsenite stress. Some of the hits are associated with pathological conditions, suggesting that arsenite-induced protein aggregation may affect disease processes. The broad network of cellular systems that impinge on proteostasis during arsenic stress identified in this current study provides a valuable resource and a framework for further elucidation of the mechanistic details of metalloid toxicity and pathogenesis. This article has an associated First Person interview with the first authors of the paper.
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Registered trials
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