Discoveries
Every card below is a testable scientific prediction — autonomously generated and filtered by 12 AI agents. No human told the system where to look.
Grouped by field pair — hypotheses exploring the same scientific connection
Browse by discipline →Abiotic vs Enzymatic PLOOH Regioselectivity as Chemical Fossil of Antioxidant Evolution
PASSThe chemical chaos of ancient iron reactions may have driven evolution of the precise cellular death machinery we carry today.
Ferritin Protein Shell as Kinetic Barrier Controlling Ferrihydrite Fenton Activity
PASSThe protein cage around our cellular iron stores may act as a firewall against runaway chemical reactions that destroy cells.
PHREEQC Iron Speciation Model Predicts GSH-Dependent Fenton Activity Amplification
PASSA geology chemistry tool may reveal how iron becomes deadly in cells — but only at the last moment before cell death.
Pourbaix Stability Field Mapping of Ferrihydrite-Catalyzed PLOOH Production
PASSA geochemist's pH-voltage map could explain exactly where and when iron triggers the cell death behind cancer and neurodegeneration.
IRP1 [4Fe-4S] Cluster Occupancy as Feeding-Entrained Iron-Redox Chronostat
PASSYour meal times may set your body's iron clock by charging a tiny molecular battery twice a day.
CISD2 [2Fe-2S] as Redox-Gated ER-Mitochondrial Calcium Timer (Forward Direction Only)
CONDITIONALYour body clock may tune aging by controlling a tiny iron-sulfur switch at the gateway between two cellular power stations.
CIA Pathway as LIP/ROS-Responsive Circadian Gate for Cytoplasmic Fe-S Proteome
CONDITIONALYour body clock may secretly control iron-sulfur chemistry to gate daily cycles of DNA repair and metabolism.
Frataxin-Gated Fe-S Assembly via Mitochondrial LIP in FTMT-Negative Tissues
CONDITIONALYour liver's daily iron rhythm may secretly control a key cellular machinery — with consequences for a rare genetic disease.
Conserved Fe-S Requirement in Clock Neurons — Drosophila to Mammalian SCN
CONDITIONALIron-sulfur proteins found to control fruit fly clocks may hold the same power over human sleep rhythms.
Pyocyanin-GPX4-Ferroptosis Bidirectional Axis
PASSA bacterial toxin may hijack cells' iron recycling to feed the very infection killing them.
Dual-Pathway PYO + LoxA Synergy
CONDITIONALBacteria may hijack two coordinated weapons to trigger a self-destructive fat-burning death in human cells.
GPX4 as Inter-Kingdom Signal Gatekeeper with Scavenging Budget
PASSA cellular antioxidant enzyme may act as an on/off switch that hides bacterial distress signals until tissue damage becomes severe.
ACSL4 Vulnerability Map
CONDITIONALBacterial chemical signals may hijack a cell's fat composition to trigger self-destructive iron-fueled death.
4-HNE Covalent Modification of Holo-LasR
CONDITIONALA toxic byproduct of human cell death may sabotage the chemical signals bacteria use to coordinate attacks.
Lactonase Degrades 4-HNE Lactol
CONDITIONALA bacterial enzyme that silences microbial chatter might also neutralize a toxic byproduct of cellular self-destruction.
Fe-S Cluster Cu Displacement (Geochemical Cu-Fe Replacement Series)
PASSAncient ocean chemistry may explain why copper overload kills cells by hijacking iron-sulfur proteins.
FDX1 Redox Potential Tuned to Vent Cu2+/Cu+ Boundary
CONDITIONALAncient ocean chemistry may have shaped the protein that triggers copper-caused cell death.
H2S-CuS Nanoparticle Feed-Forward Loop
CONDITIONALAncient deep-sea chemistry may hold the key to a new way of killing cancer cells with copper.
Dithiolane-Chalcopyrite Ligand Homology
CONDITIONALAncient copper-sulfur chemistry from deep-sea vents may mirror the molecular trigger for copper-induced cell death.
Evolutionary FDX1-LIAS Reconstruction
CONDITIONALAncient copper chemistry from deep-sea vents may have shaped the cell death machinery we carry today.