2.1.1.100: protein-S-isoprenylcysteine O-methyltransferase
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For detailed information about protein-S-isoprenylcysteine O-methyltransferase, go to the full flat file.
Word Map on EC 2.1.1.100
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2.1.1.100
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n-acetyl-s-farnesyl-l-cysteine
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cysmethynil
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medicine
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a-factor
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aax
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carboxylmethylation
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ste24p
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n-acetyl-s-geranylgeranyl-l-cysteine
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ras-driven
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biotechnology
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analysis
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drug development
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pharmacology
- 2.1.1.100
- n-acetyl-s-farnesyl-l-cysteine
- cysmethynil
- medicine
- a-factor
- aax
-
carboxylmethylation
- ste24p
- n-acetyl-s-geranylgeranyl-l-cysteine
-
ras-driven
- biotechnology
- analysis
- drug development
- pharmacology
Reaction
Synonyms
EC 2.1.1.24, farnesyl cysteine C-terminal methyltransferase, farnesyl-protein carboxymethyltransferase, farnesylated protein C-terminal O-methyltransferase, Icmt, isoprenylated protein methyltransferase, isoprenylcysteine carboxyl methyltransferase, isoprenylcysteine carboxylmethyltransferase, isoprenylcysteine carboxylmethyltransferase Ste14p, isoprenylcysteine methylesterase, methyltransferase, protein C-terminal farnesylcysteine O-, prenylated protein methyltransferase, protein S-farnesylcysteine C-terminal methyltransferase, S-farnesylcysteine methyltransferase, STE14A, STE14B, Ste14p
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analysis
biotechnology
the enzyme is a target for metabolic engineering of crop species for drought tolerance by targeted alterations in isoprenylcysteine methylation
medicine
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highly sensitive capillary electrophoresis method for monitoring of the enzymic activity
analysis
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approaches to establish the quantitative structureactivity relationship of indoloacetamides as inhibitors of ICMT
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development of Icmt inhibitors as another approach to anticancer drug development
medicine
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generation of Icmt inhibitors based on the structure of the minimal Icmt substrate N-acetyl-S-farnesyl-L-cysteine in hopes of developing potent anticancer agents
medicine
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inhibition of the enzyme results in Ras mislocalization and loss of cellular transformation ability, making it an attractive and novel anticancer target
medicine
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inhibition of the enzyme results in Ras mislocalization and loss of cellular transformation ability, making it an attractive and novel anticancer target
medicine
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a correlation exists between p53 status and ICMT expression in breast and lung cancers. ICMT overexpression is correlated with negative clinical outcomes
medicine
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
medicine
Icmt mRNA and protein levels are increased in nasopharyngeal carcinoma cells after prolonged exposure to chemotherapy. Icmt inhibition is more effective against chemoresistant compared to chemosensitive nasopharyngeal carcinoma cells. The combination of Icmt inhibition with 5-fluorouracil or cisplatin results in greater efficacy than single chemotherapeutic agent alone in nasopharyngeal carcinoma cells. Icmt inhibition decreases Ras and RhoA activities, Ras may be the critical effector of Icmt in nasopharyngeal carcinoma cells
medicine
inhibition of ICMT significantly reduces cell migration in vitro and cancer invasion and metastasis in vivo. The role of ICMT is mediated by regulator RAB4A. ICMT catalyzed carboxylmethylation is critical for RAB4A activation and interaction with effectors, its localization to endosomes and recycling vesicles, and hence important for RAB4A-dependent integrin beta3 recycling to plasma membrane
medicine
upregulation of Icmt expression is a common feature in patients with epithelial ovarian cancer regardless of age and disease stage. Ovarian cancer cell lines with higher Icmt levels are more resistant to chemotherapeutic agents. Icmt inhibition by siRNA or inhibitor cysmethynil suppresses growth and induces apoptosis in ovarian cancer cells. Icmt inhibition significantly augments chemotherapeutic agent's efficacy in vitro and in vivo. Ras activation is a critical effector of ICT in ovarian cancer cells