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Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer
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Mechanistically, NNMT suppression increased adipose SAM and NAD, upregulated polyamine flux enzymes (ODC, SSAT), and altered histone methylation consistent with a shift toward oxidative metabolism [2]
The strongest reproducible mechanism finding in the T4 literature is 1:1 binding of monomeric ATP-G-actin via the LKKTET motif at residues 17-22, with affinity in the sub-micromolar range (Safer 1991) [3]
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