EC Number   |
General Information |
Reference |
|---|
   3.4.24.59 | malfunction |
cleavage of Notch recptor at the S5 site is abolished in MIEP knockout cells |
719949 |
| 3.4.24.59 | malfunction |
down-regulation of the putative Trypanosoma brucei mitochondrial intermediate peptidase (MIP) homolog by RNAi renders the cells unable to grow after 48 hours of induction. Ablation of MIP results in the accumulation of the precursor of the trypanosomatid-specific trCOIV protein, the largest nuclear-encoded subunit of the cytochrome c oxidase complex in this flagellate |
755173 |
| 3.4.24.59 | physiological function |
Notch function can be modulated by MIPEP-mediated cleavage. Results show that S5 site proteolysis represents a novel regulatory component of Notch signaling |
719949 |
| 3.4.24.59 | physiological function |
the enzyme plays a role in stabilizing mitochondrial proteins by the removal of single amino acids from mitochondrial processing peptidase-processed proteins |
755046 |
| 3.4.24.59 | physiological function |
the stability of intermediate and mature forms of Oct1 substrate proteins in organello and in vivo is compared. Oct1 cleavage increases the half-life of its substrate proteins, most likely by re-moving destabilizing amino acids at the intermediate's N-terminus. Oct1 converts unstable precursor intermediates generated by mitochondrial processing peptidase (MPP) into stable mature proteins. Oct1 acts as a quality control system for MPP-processed preproteins |
720415 |
