EC Number   |
Protein Variants |
Reference |
|---|
   3.4.21.94 | A322T/S323N |
site-directed mutagenesis, the mutant shows unaltered activity, but slightly decreased sensitivity for inhibitor 7B2 CT peptide compared to the wild-type enzyme |
669378 |
| 3.4.21.94 | D278E |
site-directed mutagenesis of the S4/S5 subsite residue, the mutant shows altered substrate preferences, increased activity and reduced sensitivity to inhibitor 7B2 CT peptide compared to the wild-type enzyme |
669378 |
| 3.4.21.94 | L341W |
site-directed mutagenesis of the residue from the far edge of subsite S2', the mutant shows increased activity, and slightly decreased sensitivity for inhibitor 7B2 CT peptide compared to the wild-type enzyme |
669378 |
| 3.4.21.94 | more |
approximately one third of peptides found in wild-type mice are not detectable in PC2 knock-out mice, and another third are present at levels ranging from 25 to 75% of wild-type levels |
688525 |
| 3.4.21.94 | more |
EGL-3/KPC2 mutants, malprocessing of both FMRFamide-like peptide precursors and neuropeptide-like protein precursors |
-, 688526 |
| 3.4.21.94 | more |
in PC2-null mice, basal responses and responses after a cold swim are similar to wild-type mice. After a short forced swim in warm water, PC2-null mice are significantly less responsive to the stimuli than wild-type mice, an indication of increased opioid-mediated stress-induced analgesia. Enhanced analgesia in PC2-null mice may be caused by an accumulation of opioid precursor processing intermediates with potent analgesic effects, or by loss of anti-opioid peptides |
689212 |
| 3.4.21.94 | more |
islets from mice lacking PC2 and with beta-cell expression of human proIAPP develop amyloid associated with beta-cell death during 2-week culture. Rescue of PC2 expression by ex vivo transduction with Ad-PC2 restores NH(2)-terminal processing to mature IAPP and decreases both the extent of amyloid formation and the number of TUNEL-positive cells, and enhances cell survival |
686302 |
| 3.4.21.94 | more |
PC2-/- mice, brain levels of neuromedin N are reduced by more than 50% with a compensatory increase in the levels of large neuromedin N. Processing at site 2 is impaired. 20% reduction in neurotensin levels |
688466 |
| 3.4.21.94 | more |
PC2-deficient cells do not show alterations in glucose-dependent insulinotropic polypeptide precursor processing activity |
669436 |
| 3.4.21.94 | N356S |
site-directed mutagenesis of the distant prime site residue, the mutant shows altered substrate preferences compared to the wild-type enzyme |
669378 |
