https://ifosfamideinhibitor.co....m/risk-factors-linke
The mitochondrial defects upon lack of PreP derive from the accumulation of presequence peptides that trigger feedback inhibition of MPP and buildup of nonprocessed precursor proteins. Additionally, the mitochondrial advanced peptidase MIP that cleaves eight residues from a subset of precursors after MPP processing is affected upon lack of PreP suggesting that PreP also degrades MIP created octapeptides. Research regarding the PrePR183Q client mutation associated with neurologic problems unve
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