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On one hand, to sustain rapid proliferation, cancer cells actively reprogram iron metabolism pathways by upregulating iron import proteins such as TFR1 and DMT1, while downregulating the FPN, thereby increasing intracellular Fe + uptake, which in turn promotes mitochondrial function, DNA synthesis, and cell cycle progression (84)

Our work shows that single-residue mutations within the SNIP1 FHA domain that mediate association with phosphorylated SF3B1 are sufficient to disrupt optimal splicing and cellular proliferation

An American Academy of Sleep Medicine review

These mechanisms rely primarily on small-sample studies or animal models and lack in vivo mechanistic data from human subjects

Alzheimer's disease, a lipid story: involvement of peroxisome proliferator-activated receptor alpha

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