EC Number   |
General Information |
Reference |
|---|
   2.1.1.100 | malfunction |
cell migration and adhesion are impaired by enzyme inhibition (the actin cytoskeleton remains unorganized and lacks peripgeral actin filaments and stress fiber formation in the interior of the cell) |
719233 |
| 2.1.1.100 | malfunction |
enzyme inhibition reduces the function of mitochondrial oxidative phosphorylation in cancer cells. Enzyme inhibition decreases cellular ATP and depletes critical tricarboxylic acid cycle metabolites, leading to suppression of cell anabolism and growth, and marked autophagy |
734815 |
| 2.1.1.100 | malfunction |
reduced enzyme activity causes prelamin A mislocalization within the nucleus and triggers prelamin A-dependent activation of AKT-mammalian target of rapamycin signaling, which abolishes the premature senescence of Zmpste24-deficient fibroblasts. Enzyme inhibition increases AKT-mammalian target of rapamycin signaling and proliferation and delays senescence in Hutchinson-Gilford progeria syndrome fibroblasts |
735272 |
| 2.1.1.100 | malfunction |
reduced enzyme activity does not affect levels of prelamin A, but instead causes mislocalization of prelamin A away fromthe nuclear rim and triggers prelamin A-dependent activation of AKT-mTOR, which decreases premature senescence of zinc metallopeptidase STE24-deficient fibroblasts |
733905 |
| 2.1.1.100 | metabolism |
methylation of the C-terminus by Icmt is the final step in the prenylation pathway. The prenylation pathway consists of three enzymatic steps, the final processed protein is isoprenoid modified and methylated on the C-terminal cysteine. This protein modification pathway plays a significant role in cancer biology because many oncogenic proteins undergo prenylation |
704546 |
| 2.1.1.100 | metabolism |
the enzyme is involved in the farnesyl metabolism, overview |
706207 |
| 2.1.1.100 | metabolism |
the enzyme is responsible for the last common step of the posttranslational processing pathway of CaaX proteins |
719091 |
| 2.1.1.100 | physiological function |
ICMT loss-of-function isogenic cell lines for both RAS-transformed human mammary epithelial cells (HME1) and human cancer cell lines MiaPaca-2 and MDA-MB-231 containing naturally occurring mutant KRAS. In both in vitro and in vivo tumorigenesis studies, ICMT loss-of-function abolishes the tumor initiation ability of all major isoforms of mutant RAS in HME1 cells, and the tumor maintenance capacity of MiaPaca-2 and MDA-MB-231 cells |
757873 |
| 2.1.1.100 | physiological function |
isoprenylcysteine carboxylmethyltransferase plays a role in cell migration and adhesion |
719233 |
| 2.1.1.100 | physiological function |
isoprenylcysteine methylation and demethylation positively regulate abscisic acid signaling in Arabidopsis thaliana via feedback mechanism involving demethylation and inactivation of isoprenylated negative regulators of abscisic acid signaling |
706207 |
