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The pathogen protein EspF(U) hijacks actin polymerization using mimicry and multivalency

32 PTMs are mediated through two pathways: an enzymatic reaction utilizing L-lactyl-CoA as a substrate and a non-enzymatic reaction involving D-lactyl-GSH derived from methylglyoxal (MG) metabolism pathways

Potential side effects are generally mild

These agents enhance T-cell function against cancer cells by inhibiting mechanisms in the immune system that downregulate T-cell activity

Therefore, combining therapy targeting the MYC pathway with intervention in glutamine metabolism should be key to reversing MYC-driven tumor growth and restoring the antitumor immune response

It protects our DNA, cell lipids, and proteins from free radicals and oxidative stress