Fungi - Candida albicans - Research News, Data, Publications & Aproaches - ERG11 Mutations - Telomeres - Nuclear Biology & Nuclear Chemistry Aproaches - Heme-Dependant Nuclear Chemistry - Non-Elaborate Posts - Post 3
Unlike cytoplasmic P450 systems, ERG11 operates in a nuclear context subject to dynamic oxidative gradients. The nucleus of C. albicans is not redox-inert; rather, it maintains a regulated oxidative potential mediated by thioredoxin-like proteins, nuclear glutathione pools, and ROS-buffering heme oxygenases.
When antifungal azoles disrupt the ERG11 enzyme, the accumulation of lanosterol intermediates elevates ROS generation, which diffuses into the nucleus and perturbs redox-sensitive transcription factors such as Cap1p and Hap43p. This feedback loop couples enzymatic electron flow with the nuclear oxidative landscape, transforming a chemical reaction into a genomic signal. The result is a self-referential circuit: the redox chemistry of ERG11 modulates its own transcription through oxidative communication.
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