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This selectivity is attributed to its utilization of PepT1, a transporter upregulated during inflammatory states, suggesting KPV's potential interest as a research subject in the context of inflammatory bowel disease (IBD)

These sites are cleaved by the AP endonuclease, APE1, and corresponding nucleotides are then located into the gap by a DNA polymerase through two different sub-pathways, to finally be ligated by a DNA ligase (Krokan and Bjoras, 2013)