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This dominantly inherited syndrome is caused by pathogenic variants in the genes responsible for DNA mismatch repair (MMR), i.e., MLH1, MSH2, MSH6, or PMS2, or in the EPCAM gene (leading to the silencing of the MSH2 gene) [4]

TMAO levels significantly associated with the quantitative abundance of 65 bacterial species (corrected for bacterial load) in BMIS individuals after correcting for demographics and BMI, primarily (44/65) of the Firmicutes phylum (Fig

Absorbance was measured using a microplate spectrophotometer, and the concentrations were calibrated based on the standard curve provided by the assay kit

3-mercaptopyruvate sulfurtransferase (MPST, EC 2.8.1.2), another enzyme with known rhodanese activity, is evolutionarily believed to be closely linked to TST because of its high sequence homology