ArticleMolecular biology of the cell2011
Btn3 is a negative regulator of Btn2-mediated endosomal protein trafficking and prion curing in yeast.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- The Lack of a COPII Cargo Receptor Erv14 Impacts Physiological Functions of the Vacuole in Saccharomyces cerevisiae.Traffic (Copenhagen, Denmark) · 2026Article
- Anti-Prion Systems in Saccharomyces cerevisiae.Journal of neurochemistry · 2025Review
- Improving therapeutic protein secretion in the probiotic yeast Saccharomyces boulardii using a multifactorial engineering approach.Microbial cell factories · 2023Article
- The HOPS tethering complex is required to maintain signaling endosome identity and TORC1 activity.The Journal of cell biology · 2022Article
- Article
- Innate immunity to prions: anti-prion systems turn a tsunami of prions into a slow drip.Current genetics · 2021Review
- Proteasome Control of [URE3] Prion Propagation by Degradation of Anti-Prion Proteins Cur1 and Btn2 in Saccharomyces cerevisiae.Genetics · 2021Article
- Article
- Normal levels of ribosome-associated chaperones cure two groups of [PSI+] prion variants.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cellular models of Batten disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- How Do Yeast Cells Contend with Prions?International journal of molecular sciences · 2020Review
- Anti-prion systems in yeast.The Journal of biological chemistry · 2019Review
- Engineering the protein secretory pathway ofProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cdc48 and ubiquilins confer selective anterograde protein sorting and entry into the multivesicular body in yeast.Molecular biology of the cell · 2018Article
- Anti-Prion Systems in Yeast and Inositol Polyphosphates.Biochemistry · 2018Article
- Nonsense-mediated mRNA decay factors cure most [PSI+] prion variants.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Yeast and Fungal Prions.Cold Spring Harbor perspectives in biology · 2016Review
- Yeast prions: structure, biology, and prion-handling systems.Microbiology and molecular biology reviews : MMBR · 2015Review
- Dynamic droplets: the role of cytoplasmic inclusions in stress, function, and disease.Cellular and molecular life sciences : CMLS · 2015Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yeast Btn2 facilitates the retrieval of specific proteins from late endosomes (LEs) to the Golgi, a process that may be adversely affected in Batten disease patients. We isolated the putative yeast orthologue of a human complex I deficiency gene, designated here as BTN3, as encoding a Btn2-interacting protein and negative regulator. First, yeast overexpressing BTN3 phenocopy the deletion of BTN2 and mislocalize certain trans-Golgi proteins, like Kex2 and Yif1, to the LE and vacuole, respectively. In contrast, the deletion of BTN3 results in a tighter pattern of protein localization to the Golgi. Second, BTN3 overexpression alters Btn2 localization from the IPOD compartment, which correlates with a sharp reduction in Btn2-mediated [URE3] prion curing. Third, Btn3 and the Snc1 v-SNARE compete for the same binding domain on Btn2, and this competition controls Btn2 localization and function. The inhibitory effects upon protein retrieval and prion curing suggest that Btn3 sequesters Btn2 away from its substrates, thus down-regulating protein trafficking and aggregation. Therefore Btn3 is a novel negative regulator of intracellular protein sorting, which may be of importance in the onset of complex I deficiency and Batten disease in humans.
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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.