The C-terminal tail of polycystin-1 suppresses cystic disease in a mitochondrial enzyme-dependent fashion - Nature Communications

. Our observation that CTT-dependent changes in cellular redox are associated with increases in both NADH and NADPH levels is somewhat surprising and is not entirely consistent with the predictions of either the forward or reverse-mode models.

In summary, we have identified an interaction between the mitochondrial enzyme NNT and the C-terminal tail of PC1 . More importantly, we showed that expressing the 200 aa C-terminal tail of PC1 in a-KO murine model of ADPKD is capable of significantly suppressing the cystic phenotype in an NNT-dependent fashion. Recent data shows that re-expression of full-length PC1 in a.

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