ArticleCell death & disease2012
14-3-3 protects against stress-induced apoptosis.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
- Exploring 14-3-3ζ: insights into its role in cancer mechanisms and future therapeutic applications.Hereditas · 2026Review
- Multilineage-differentiating stress-enduring cells: a powerful tool for tissue damage repair.Frontiers in cell and developmental biology · 2024Review
- The yeast 14-3-3 proteins Bmh1 and Bmh2 regulate key signaling pathways.Frontiers in molecular biosciences · 2024Review
- Muse cells: ushering in a new era of stem cell-based therapy for stroke.Stem cell research & therapy · 2022Review
- Yeast as a tool to decipher the molecular mechanisms underlying the functions of Bcl-2 family.Exploration of targeted anti-tumor therapy · 2022Review
- Creating a Selective Nanobody Against 3-Nitrotyrosine Containing Proteins.Frontiers in chemistry · 2022Article
- Mesenchymal Stem Cell-Derived Extracellular Vesicles to the Rescue of Renal Injury.International journal of molecular sciences · 2021Review
- Article
- Genome-Scale Screening and Combinatorial Optimization of Gene Overexpression Targets to Improve Cadmium Tolerance inFrontiers in microbiology · 2021Article
- Intelligent Design of 14-3-3 Docking Proteins Utilizing Synthetic Evolution Artificial Intelligence (SYN-AI).ACS omega · 2019Article
- Selective 14-3-3γ Upregulation Promotes Beclin-1-LC3-Autophagic Influx via β-Catenin Interaction in Starved Neurons In Vitro and In Vivo.Neurochemical research · 2019Article
- Differential abundance and transcription of 14-3-3 proteins during vegetative growth and sexual reproduction in budding yeast.Scientific reports · 2018Article
- HucMSC exosomes-delivered 14-3-3ζ enhanced autophagy via modulation of ATG16L in preventing cisplatin-induced acute kidney injury.American journal of translational research · 2018Article
- The secretome of MUSE cells contains factors that may play a role in regulation of stemness, apoptosis and immunomodulation.Cell cycle (Georgetown, Tex.) · 2017Article
- Heterologous expression of anti-apoptotic human 14-3-3β/α enhances iron-mediated programmed cell death in yeast.PloS one · 2017Article
- Combined Antibody/Lectin Enrichment Identifies Extensive Changes in the O-GlcNAc Sub-proteome upon Oxidative Stress.Journal of proteome research · 2016Article
- External and internal triggers of cell death in yeast.Cellular and molecular life sciences : CMLS · 2016Review
- miR-185 mediates lung epithelial cell death after oxidative stress.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Mitochondrial proteomics of the acetic acid - induced programmed cell death response in a highly tolerantMicrobial cell (Graz, Austria) · 2016Article
- Functional analysis of Paracoccidioides brasiliensis 14-3-3 adhesin expressed in Saccharomyces cerevisiae.BMC microbiology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Expression of human Bax, a cardinal regulator of mitochondrial membrane permeabilization, causes death in yeast. We screened a human cDNA library for suppressors of Bax-mediated yeast death and identified human 14-3-3β/α, a protein whose paralogs have numerous chaperone-like functions. Here, we show that, yeast cells expressing human 14-3-3β/α are able to complement deletion of the endogenous yeast 14-3-3 and confer resistance to a variety of different stresses including cadmium and cycloheximide. The expression of 14-3-3β/α also conferred resistance to death induced by the target of rapamycin inhibitor rapamycin and by starvation for the amino acid leucine, conditions that induce autophagy. Cell death in response to these autophagic stimuli was also observed in the macroautophagic-deficient atg1Δ and atg7Δ mutants. Furthermore, 14-3-3β/α retained its ability to protect against the autophagic stimuli in these autophagic-deficient mutants arguing against so called 'autophagic death'. In line, analysis of cell death markers including the accumulation of reactive oxygen species, membrane integrity and cell surface exposure of phosphatidylserine indicated that 14-3-3β/α serves as a specific inhibitor of apoptosis. Finally, we demonstrate functional conservation of these phenotypes using the yeast homolog of 14-3-3: Bmh1. In sum, cell death in response to multiple stresses can be counteracted by 14-3-3 proteins.
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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.