ArticlemSphere2021
A Suppressor Mutation in the β-Subunit Kis1 Restores Functionality of the SNF1 Complex in
Article in mSphere, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Inducible gene deletion reveals essentiality of protein kinases and a septation initiation network in Candida albicans.PLoS genetics · 2026Article
- Adh1-Programmed SNF1 Phosphogradients Decrypt Morphogenesis in Candida albicans: Chemical Interrogation Unveils Hyphal Transition Thresholds.Microbial biotechnology · 2026Article
- Article
- The Ypk1 protein kinase signaling pathway is rewired and not essential for viability in Candida albicans.PLoS genetics · 2023Article
- Glucose-enhanced oxidative stress resistance-A protective anticipatory response that enhances the fitness of Candida albicans during systemic infection.PLoS pathogens · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterotrimeric protein kinase SNF1 is a key regulator of metabolic adaptation in the pathogenic yeast Candida albicans, and mutants with a defective SNF1 complex cannot grow on carbon sources other than glucose. We identified a novel type of suppressor mutation in the β-subunit Kis1 that rescued the growth defects of cells lacking the regulatory γ-subunit Snf4 of the SNF1 complex. Unlike wild-type Kis1, the mutated Kis1
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Registered trials
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