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Further in vitro studies have shown that IAA can promote epithelial cell proliferation and enhance tight junction repair by activating the AhR/IL-22 signaling pathway, thereby counteracting LPS-induced epithelial injury and preventing LPS-driven systemic inflammation 168

However, in case of the ASCT2, studies showed that cysteine is actually a competitive inhibitor and not a substrate for ASCT2 ( Figure 1 via Multidrug Resistance Protein 1 exporter (MRP1), is cleaved extracellularly by -Glutamyl transferase (GGT) forming -Glutamyl-X substrate and Cysteinyl-Glycine

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Carcinogenesis 4:11931195