EC Number   |
General Information |
Reference |
|---|
   2.5.1.59 | evolution |
tunable selectivity may be a general phenomenon among multispecific enzymes involved in posttranslational modification and raises the possibility of variable substrate selectivity among GGTase-I orthologues from different organisms |
737695 |
| 2.5.1.59 | malfunction |
combined FTase/GGTase-I deficiency significantly reduces K-Ras-induced lung tumors and improves survival without obvious pulmonary toxicity |
738097 |
| 2.5.1.59 | malfunction |
downregulation or inhibition of GGT decreases synaptogenesis |
-, 738895 |
| 2.5.1.59 | malfunction |
GGTase-I inhibition results in proliferation inhibition associated with G1 arrest and accumulation of cell cycle regulators such as p21CIP1/WAF1 |
739426 |
| 2.5.1.59 | malfunction |
high K+ or bicuculline-induced increases in dendritic spine density are significantly abolished by enzyme inhibition. GGTI not only regulates the basal neuronal dendritic growth but also mediates neuronal activity and BDNF-induced dendritogenesis. Dendrite development of Purkinje cells is dramatically impeded by downregulation of GGTIbeta expression or inhibiting GGTI activity in cultured cerebellar slices |
739114 |
| 2.5.1.59 | malfunction |
loss of enzyme activity results in colonies of round, single-celled organisms that resemble unicellular algae. Enzyme mutants fail to respond to polarized light. Ppggb mutants appear to remain in an undifferentiated state, with no sign of polarity |
739309 |
| 2.5.1.59 | malfunction |
mice with lateral ventricular injection of GGTi-2147, a specific GGTI inhibitor, have significant reduction in the membrane association of Rac1 and in the dendritic spine densities in the hippocampus, the cerebellum, and the frontal cortex |
739114 |
| 2.5.1.59 | malfunction |
overexpression of GGTbeta promotes the linear density of post-synaptic density protein 95 (PSD 95) and synapsin 1, two major molecular markers of synaptogenesis, while downregulation or inhibition of GGT decreases synaptogenesis |
-, 738895 |
| 2.5.1.59 | malfunction |
the related Rac and Ras proteins are not mislocalized in the cdc43DELTA mutant even though they contain similar CaaL motifs, the membrane localization of each of these GTPases is dependent on the prenylation of the CaaX cysteine. The cdc43DELTA mutant has a growth defect at 37°C and 39°C. The cdc43dELTA mutant does not exhibit cell wall defects. The cdc43DELTA mutant is more susceptible to farnesyltransferase inhibitors |
738142 |
| 2.5.1.59 | more |
FTase and GGTase-I recognize the same CAAX sequence motif in a protein substrate and catalyze the attachment of farnesyl and geranygeranyl groups to the protein, respectively. The X is the key residue that determines the farnesylation or geranylgeranylation of the CAAX-containing protein. When X is serine, methionine or glutamine the protein substrate is preferentially activated by FTase, but when X is leucine or phenylalanine the protein substrate is preferentially activated by GGTase-I |
738097 |
