ArticleFrontiers in genetics2013
The cellular roles of Ccr4-NOT in model and pathogenic fungi-implications for fungal virulence.
Article in Frontiers in genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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
16 citing papers in PubMed, 26 citations in OpenAlex.
- ThemSphere · 2025Article
- Article
- Post-transcriptional control of fungal cell wall synthesis.Cell surface (Amsterdam, Netherlands) · 2022Article
- TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV.Nature communications · 2022Article
- The Combination of Iron and Copper Increases Pathogenicity and Induces Proteins Related to the Main Virulence Factors in Clinical Isolates ofJournal of fungi (Basel, Switzerland) · 2022Article
- Deciphering the Dynamics of Signaling Cascades and Virulence Factors ofMicroorganisms · 2021Article
- Article
- Mutations in theFrontiers in genetics · 2017Article
- Building on the Ccr4-Not architecture.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Article
- The Ccr4-Not complex is a key regulator of eukaryotic gene expression.Wiley interdisciplinary reviews. RNA · 2016Review
- Post-transcriptional gene regulation in the biology and virulence of Candida albicans.Cellular microbiology · 2016Review
- CCR4-Not Complex Subunit Not2 Plays Critical Roles in Vegetative Growth, Conidiation and Virulence in Watermelon Fusarium Wilt PathogenFrontiers in microbiology · 2016Article
- The FgNot3 Subunit of the Ccr4-Not Complex Regulates Vegetative Growth, Sporulation, and Virulence in Fusarium graminearum.PloS one · 2016Article
- Modifiers of solid RNP granules control normal RNP dynamics and mRNA activity in early development.The Journal of cell biology · 2015Article
- PAT-seq: a method to study the integration of 3'-UTR dynamics with gene expression in the eukaryotic transcriptome.RNA (New York, N.Y.) · 2015Article
- Multifunctional roles of the mammalian CCR4-NOT complex in physiological phenomena.Frontiers in genetics · 2014Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
The fungal Ccr4-NOT complex has been implicated in orchestrating gene expression networks that impact on pathways key for virulence in pathogenic species. The activity of Ccr4-NOT regulates cell wall integrity, antifungal drug susceptibility, adaptation to host temperature, and the developmental switches that enable the formation of pathogenic structures, such as filamentous hyphae. Moreover, Ccr4-NOT impacts on DNA repair pathways and genome stability, opening the possibility that this gene regulator could control adaptive responses in pathogens that are driven by chromosomal alterations. Here we provide a synthesis of the cellular roles of the fungal Ccr4-NOT, focusing on pathways important for virulence toward animals. Our review is based on studies in models yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, and two species that cause serious human infections, Candida albicans and Cryptococcus neoformans. We hypothesize that the activity of Ccr4-NOT could be targeted for future antifungal drug discovery, a proposition supported by the fact that inactivation of the genes encoding subunits of Ccr4-NOT in C. albicans and C. neoformans reduces virulence in the mouse infection model. We performed bioinformatics analysis to identify similarities and differences between Ccr4-NOT subunits in fungi and animals, and discuss this knowledge in the context of future antifungal strategies.
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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.