EC Number   |
Natural Substrates |
|---|
   2.1.1.100 | more |
overexpression of the enzyme may protect against endothelial cell apoptosis by enhancing, the carboxyl methylation posttranslational modification, activity, and subsequent intracellular signalling pathway of Ras GTPase |
| 2.1.1.100 | more |
the enzyme regulates Rac1 activity by controlling the interaction of Rac1 activity by controlling the interaction of Rac1 with Rho guanine nucleotide dissociation inhibitor, the enzyme regulates membrane accumulation and GTP loading of Rac1 |
| 2.1.1.100 | more |
inhibition of Icmt significantly decreases the activation of both RhoA and Rac1 involving Rho GDP-dissociation inhibitor, RhoGDI, overview. Icmt inhibition impairs RhoGTPase activation |
| 2.1.1.100 | more |
the ICMT isozyme catalyzes the methylation of C-terminal isoprenylcysteines |
| 2.1.1.100 | S-adenosyl-L-methionine + (RhoAA) C-terminal S-farnesyl-L-cysteine |
the enzyme modulates endothelial monolayer per meability by altering RhoA carboxyl methylation and activation, thus changing the organization of intercellular junctions. Carboxy methylation of RhoA may modulate endothelial barrier function |
| 2.1.1.100 | S-adenosyl-L-methionine + protein C-terminal S-farnesyl-L-cysteine |
- |
| 2.1.1.100 | S-adenosyl-L-methionine + protein C-terminal S-farnesyl-L-cysteine |
carboxyl methylation may play a role in the regulation of receptor mediated signal transduction processes in eukaryotic cells |
| 2.1.1.100 | S-adenosyl-L-methionine + protein C-terminal S-farnesyl-L-cysteine |
a-factor mating pheromone, Ras1 and Ras2 are putative substrates of the enzyme |
| 2.1.1.100 | S-adenosyl-L-methionine + protein C-terminal S-farnesyl-L-cysteine |
reversible methylation of ras-proteins may play an important role in the modulation of their signaling properties |
| 2.1.1.100 | S-adenosyl-L-methionine + protein C-terminal S-farnesyl-L-cysteine |
the protein is involved in posttranslational modifications of Ras proteins |
