ArticleProceedings of the National Academy of Sciences of the United States of America2006
Ras pathway signaling accelerates programmed cell death in the pathogenic fungus Candida albicans.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 146 citations in OpenAlex.
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- An integrative ultrastructural and transcriptomic analysis of host-pathogen interactions with human brain microvascular endothelial cells during cryptococcal infection: a preliminary study.Frontiers in cellular and infection microbiology · 2026Article
- Antifungal persistence: Clinical relevance and mechanisms.PLoS pathogens · 2025Review
- Anti-Candidal Efficacy of Alternative Natural Formulations as a Denture Cleansing Agent - Is Ayurveda the Answer? - AnJournal of pharmacy & bioallied sciences · 2025Article
- Intratumor fungi specific mechanisms to influence cell death pathways and trigger tumor cell apoptosis.Cell death discovery · 2025Review
- Current and novel approaches in yeast cell death research.Cell death and differentiation · 2025Review
- Developing novel antifungals: lessons from G protein-coupled receptors.Trends in pharmacological sciences · 2023Review
- The Cdc25 and Ras1 Proteins ofJournal of fungi (Basel, Switzerland) · 2023Article
- Roles of the pro-apoptotic factors CaNma111 and CaYbh3 in apoptosis and virulence of Candida albicans.Scientific reports · 2022Article
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- Underlying mechanisms of the effect of minocycline againstExperimental and therapeutic medicine · 2021Article
- Growth modulation and metabolic responses of Ganoderma boninense to salicylic acid stress.PloS one · 2021Article
- Regulation of Cell Death Induced by Acetic Acid in Yeasts.Frontiers in cell and developmental biology · 2021Review
- Review
- Pkh1p-Ypk1p and Pkh1p-Sch9p Pathways Are Activated by Acetic Acid to Induce a Mitochondrial-Dependent Regulated Cell Death.Oxidative medicine and cellular longevity · 2020Article
- Iron Chelator Deferasirox ReducesAntimicrobial agents and chemotherapy · 2019Article
- Non-Toxic and Ultra-Small Biosilver Nanoclusters Trigger Apoptotic Cell Death in Fluconazole-ResistantBiomolecules · 2019Article
- Candida albicans Ras1 Inactivation Increases Resistance to Phagosomal Killing by Human Neutrophils.Infection and immunity · 2018Article
- Fungal persister cells: The basis for recalcitrant infections?PLoS pathogens · 2018Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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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
A better understanding of the molecular basis of programmed cell death (PCD) in fungi could provide information that is useful in the design of antifungal drugs that combat life-threatening fungal infections. Harsh environmental stresses, such as acetic acid or hydrogen peroxide, have been shown to induce PCD in the pathogenic fungus Candida albicans. In this study, we show that dying cells progress from an apoptotic state to a secondary necrotic state and that the rate at which this change occurs is proportional to the intensity of the stimulus. Also, we found that the temporal response is modulated by Ras-cAMP-PKA signals. Mutations that block Ras-cAMP-PKA signaling (ras1Delta, cdc35Delta, tpk1Delta, and tpk2Delta) suppress or delay the apoptotic response, whereas mutations that stimulate signaling (RAS1(val13) and pde2Delta) accelerate the rate of entry of cells into apoptosis. Pharmacological stimulation or inhibition of Ras signaling reinforces these findings. Transient increases in endogenous cAMP occur under conditions that stimulate apoptosis but not growth arrest. Death-specific changes in the abundance of different isoforms of the PKA regulatory subunit, Bcy1p, are also observed. Activation of Ras signals may regulate PCD of C. albicans, either by inhibiting antiapoptotic functions (such as stress responses) or by activating proapoptotic functions.
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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.