Affinage

ICMT

Protein-S-isoprenylcysteine O-methyltransferase · UniProt O60725

Length
284 aa
Mass
31.9 kDa
Annotated
2026-06-10
38 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ICMT is the terminal enzyme of CAAX protein processing, an integral endoplasmic reticulum membrane methyltransferase that catalyzes SAM-dependent carboxyl methylation of the C-terminal isoprenylcysteine of prenylated proteins, thereby controlling their membrane association and downstream signaling (PMID:16757321). Structural and kinetic work defines the catalytic logic: an unusual fold built from transmembrane helices with a C-terminal cofactor pocket and a lipid tunnel that connects the reactive SAM methyl group to the membrane-embedded prenyl substrate (PMID:22195972), with an active site spanning cytosolic and membrane-exposed regions that provides separate entry routes for the cytosolic methyl donor and the ER-associated prenylcysteine (PMID:29342140, PMID:25059662); catalysis follows an ordered sequential mechanism in which SAM binds first and AdoHcy is released last (PMID:15625008). ICMT is the sole enzyme methylating isoprenylated CAAX proteins including all four RAS isoforms, and loss of methylation mislocalizes RAS away from the plasma membrane (PMID:16757321); NRAS is uniquely ICMT-dependent because methylation promotes its palmitoylation, PDE6δ binding, and anterograde Golgi-to-membrane trafficking (PMID:33579760). Through these substrates ICMT supports oncogenic signaling—its inactivation blocks K-Ras and B-Raf transformation by accelerating RhoA turnover and elevating p21(Cip1) via Ras/Erk (PMID:14966563), and it is required for Ras/Raf/Mek/Erk-driven signaling and substrate membrane targeting in multiple cancer contexts including the BRAFV600E-driven, INPP5E-dependent program (PMID:31451223, PMID:42127111). ICMT also methylates substrates in specialized tissues, including transducin and cone PDE6 in photoreceptors where its retinal loss disrupts phototransduction (PMID:27147662), and its expression is transcriptionally repressed by wild-type p53 and elevated by cancer-associated p53 mutants (PMID:30655292).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2004 High

    Established the catalytic mechanism of ICMT, defining how a single enzyme coordinates a hydrophilic cofactor and a lipophilic prenyl substrate.

    Evidence In vitro enzyme kinetics with synthetic substrate BFC, dead-end and product inhibition studies

    PMID:15625008

    Open questions at the time
    • Kinetics performed on a synthetic small-molecule substrate, not full-length prenylated proteins
    • Does not localize the substrate-binding residues structurally
  2. 2004 High

    Demonstrated that ICMT is functionally required for oncogenic transformation, connecting CAAX methylation to a defined RhoA/p21(Cip1) growth-control pathway.

    Evidence Conditional Icmt knockout in mouse fibroblasts; soft agar, xenograft, and p21(Cip1) double-knockout rescue

    PMID:14966563

    Open questions at the time
    • Mechanism by which methylation loss accelerates RhoA turnover not resolved
    • Did not identify all relevant methylated substrates contributing to transformation block
  3. 2006 Medium

    Established ICMT as the unique enzyme methylating isoprenylated CAAX proteins and showed methylation controls RAS membrane localization.

    Evidence Conditional Icmt knockout, subcellular fractionation, and electrophoretic mobility shift assays

    PMID:16757321

    Open questions at the time
    • Data compiled in a methods review from a single lab
    • Quantitative contribution of methylation versus prenylation to localization not separated
  4. 2011 High

    Provided the first structural framework for the ICMT fold, explaining how transmembrane helices and a lipid tunnel accommodate both SAM and a prenyl substrate.

    Evidence X-ray crystallography of a prokaryotic ICMT ortholog

    PMID:22195972

    Open questions at the time
    • Prokaryotic ortholog may differ from the human enzyme in detail
    • No bound prenylcysteine substrate captured
  5. 2014 High

    Mapped catalytic and substrate-binding residues across the enzyme, confirming the active site spans cytosolic and membrane-embedded regions.

    Evidence Scanning mutagenesis of ~half of all residues in the Anopheles gambiae ortholog with methyltransferase assays

    PMID:25059662

    Open questions at the time
    • Performed on an insect ortholog rather than the human enzyme
    • Functional effects inferred from activity loss without structural confirmation at the time
  6. 2016 High

    Showed ICMT is required for photoreceptor function via methylation of phototransduction substrates, distinguishing methylation-dependent from -AAX-dependent trafficking.

    Evidence Retina-specific conditional Icmt knockout mice; electroretinography; subcellular fractionation; epistatic comparison with Rce1

    PMID:27147662

    Open questions at the time
    • Mechanism linking methylation loss to reduced substrate protein levels unclear
    • Does not establish direct methylation of each affected substrate in vivo
  7. 2018 High

    Delivered a high-resolution eukaryotic ICMT structure with cofactor and lipid bound, defining distinct entry routes for SAM and prenylcysteine substrates.

    Evidence X-ray crystallography at 2.3 Å with monobody-assisted crystallization, SAM and ordered lipid bound

    PMID:29342140

    Open questions at the time
    • No bound CAAX peptide substrate to define the prenylcysteine-binding mode directly
    • Conformational dynamics of catalysis not captured by a static structure
  8. 2019 Medium

    Identified p53-dependent transcriptional control of ICMT, with opposite regulation by wild-type versus mutant p53.

    Evidence ChIP assay, promoter-luciferase reporters, truncation analysis, p53 overexpression/knockdown

    PMID:30655292

    Open questions at the time
    • Single lab; mutant-p53 activating mechanism on a distinct promoter region not fully defined
    • Physiological consequences of p53-driven ICMT changes not established
  9. 2019 Medium

    Validated ICMT pharmacologically as a target whose inhibition impairs RAS membrane association and signaling and kills Ras-mutant tumors.

    Evidence ICMT inhibitor UCM-1336; enzymatic assay, fractionation, Ras-GTP pull-down, viability assays, in vivo AML model; plus HCC siRNA/overexpression studies of Ras/Raf/Mek/Erk and EMT

    PMID:31181882 PMID:31451223

    Open questions at the time
    • Off-target effects of inhibitors on other methylated substrates not excluded
    • HCC studies lack direct methylation readout
  10. 2021 High

    Explained why NRAS is uniquely ICMT-dependent—methylation enables its palmitoylation, PDE6δ binding, and Golgi-to-membrane trafficking.

    Evidence ICMT knockout cells; FRAP/photoactivation of GFP-NRAS; PDE6δ Co-IP; palmitoylation assays; fractionation

    PMID:33579760

    Open questions at the time
    • Quantitative coupling between methylation and palmitoylation enzymes not defined
    • Generality to other single-palmitoylation CAAX proteins untested
  11. 2021 High

    Demonstrated therapeutic potential of targeting ICMT in progeria, with rigorous specificity controls.

    Evidence HGPS mice with Icmt knockout; ICMT inhibitor C75; proliferation/senescence assays; Zmpste24/Icmt double-knockout controls

    PMID:33526168

    Open questions at the time
    • Direct measurement of prelamin A methylation status not reported here
    • Long-term consequences of systemic ICMT inhibition unaddressed
  12. 2022 Medium

    Identified PFKFB4 as a physical partner that enhances ICMT/RAS interaction and RAS localization, revealing a non-glycolytic input to ICMT function.

    Evidence Co-IP of PFKFB4-ICMT; RAS localization; AKT phosphorylation; migration assays; PFKFB4 knockdown/overexpression

    PMID:35914811

    Open questions at the time
    • Single Co-IP without reciprocal validation of direct binding
    • Whether PFKFB4 modulates ICMT catalytic activity directly is unknown
  13. 2024 Medium

    Linked ICMT overexpression to invasive cell behavior, implicating its substrates in actin-based invadopodia and metastasis.

    Evidence ICMT overexpression in cancer cells; invadopodia assay; in vivo lung metastasis model; migration/invasion assays

    PMID:38301884

    Open questions at the time
    • Specific methylated substrate driving invadopodia not identified
    • Single-lab gain-of-function without loss-of-function corroboration in the same model
  14. 2026 High

    Identified INPP5E as an ICMT-dependent substrate mediating BRAFV600E-driven tumor growth through membrane targeting and PI(4,5)P2 control.

    Evidence Genetic and pharmacologic ICMT inhibition; INPP5E methylation assay; fractionation; PI(4,5)P2 measurement; forced membrane targeting rescue; xenografts

    PMID:42127111

    Open questions at the time
    • Rescue was only partial, implying additional substrates contribute
    • Precise lipid-signaling node downstream of PI(4,5)P2 not delineated
  15. 2025 Medium

    Connected ICMT-dependent RAC1 methylation to BRAF-inhibitor resistance via TAZ nuclear translocation, defining a combination-therapy rationale.

    Evidence RAC1 prenylation-site mutant; cysmethynil plus MAPK inhibitors; in vitro/in vivo tumor assays; TAZ localization and rescue (preprint)

    PMID:bio_10.1101_2025.08.10.669587

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Direct methylation of RAC1 by ICMT not biochemically demonstrated here
    • Generality beyond RAC1(P29S) resistance unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How methylation status is dynamically read by downstream trafficking machinery and chaperones to dictate substrate fate across tissues remains incompletely defined.
  • No structure with a bound full-length CAAX substrate
  • Mechanism coupling methylation to palmitoylation and PDE6δ handoff not resolved at molecular detail
  • Complete substrate repertoire and tissue-specific dependencies not catalogued

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 3 GO:0008289 lipid binding 2
Localization
GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-392499 Metabolism of proteins 2
Partners
INPP5EKRASNRASPDE6DPFKFB4RAC1RHOA

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 Crystal structure of a prokaryotic ICMT ortholog revealed a markedly different architecture from conventional methyltransferases: a core of five transmembrane α-helices with a cofactor-binding pocket in a conserved C-terminal catalytic subdomain, and a tunnel linking the reactive methyl group of SAM to the inner membrane providing access for the prenyl lipid substrate, explaining how the enzyme accommodates both a hydrophilic cofactor (SAM) and a lipophilic prenyl substrate. X-ray crystallography of prokaryotic ICMT ortholog Molecular cell High 22195972
2018 X-ray structure of eukaryotic ICMT at 2.3 Å (in complex with SAM cofactor, an ordered lipid molecule, and a monobody inhibitor) revealed that the active site spans cytosolic and membrane-exposed regions, indicating distinct entry routes for the cytosolic methyl donor SAM and for prenylcysteine substrates associated with the ER membrane. X-ray crystallography at 2.3 Å resolution with monobody-assisted crystallization Nature High 29342140
2004 Human ICMT catalysis proceeds through an ordered sequential kinetic mechanism in which SAM binds first and S-adenosylhomocysteine (AdoHcy) is the final product released; the prenylcysteine substrate (BFC) and its methylated product bind different enzyme forms, established using dead-end inhibitor (FTA) and product inhibition studies. In vitro enzyme kinetics with synthetic substrate BFC, dead-end inhibitor analysis, and product inhibition studies BMC biochemistry High 15625008
2014 Scanning mutagenesis of nearly half the residues of the Anopheles gambiae ICMT ortholog combined with methyltransferase assays identified 62 mutations causing reduced or undetectable catalytic activity; residues in transmembrane regions contribute to the isoprenylcysteine binding site (certain substitutions caused substrate inhibition by isoprenylcysteine), while the AdoMet-binding site resembles a distantly related prokaryotic methyltransferase, establishing that the active site spans cytosolic and membrane-embedded regions. Scanning mutagenesis combined with in vitro methyltransferase assays; structural comparison with Ma MTase crystal structure The Journal of biological chemistry High 25059662
2004 Genetic inactivation of Icmt in mouse fibroblasts expressing oncogenic K-Ras inhibited K-Ras-induced oncogenic transformation (soft agar and nude mice); the mechanism involved accelerated RhoA protein turnover leading to reduced RhoA levels and a large Ras/Erk1/2-dependent increase in p21(Cip1); deletion of p21(Cip1) restored growth in soft agar of Icmt-null K-Ras cells. Icmt inactivation also blocked transformation by oncogenic B-Raf(V599E). Conditional Cre-lox knockout of Icmt in mouse embryonic fibroblasts; soft agar assay; nude mouse xenograft; p21(Cip1) double knockout rescue experiment; Western blot for Erk1/2, Akt1, RhoA The Journal of clinical investigation High 14966563
2006 ICMT is the only enzyme in mouse cells capable of methylating isoprenylated CAAX proteins including all Ras proteins; in the absence of carboxyl methylation, Ras proteins are mislocalized away from the plasma membrane and exhibit a shift in electrophoretic mobility. Additionally, ICMT methylates the CXC class of isoprenylated Rab proteins. Genetic knockout (conditional Icmt deletion), subcellular fractionation, electrophoretic mobility shift assays Methods in enzymology Medium 16757321
2021 Among the four RAS proteins, NRAS uniquely requires ICMT for delivery to the plasma membrane; this is because NRAS has only a single palmitoylation site as its secondary membrane-affinity module. ICMT-dependent carboxyl methylation of NRAS promotes efficient palmitoylation, binding to the prenyl-protein chaperone PDE6δ, and anterograde trafficking from the Golgi to the plasma membrane. FRAP of GFP-NRAS revealed increased Golgi flux in the absence of ICMT, independent of palmitoylation. ICMT knockout cells; photoactivation and FRAP of GFP-NRAS; Co-IP/binding assay with PDE6δ; palmitoylation assays; subcellular fractionation Life science alliance High 33579760
2016 Retina-specific knockout of Icmt in mice caused progressive loss of rod and cone light-mediated responses, accompanied by defective association of isoprenylated transducin and cone phosphodiesterase 6 (PDE6α') with photoreceptor membranes, and decreased protein levels of transducin, PDE6α', and cone GRK1. Unlike Rce1 deficiency, rod PDE6 trafficked normally to the outer segment in Icmt-deficient mice, indicating that the -AAX (not methylation) blocks PDE6 transport. Retina-specific conditional Icmt knockout mice; electroretinography; subcellular fractionation; protein level quantification by Western blot The Journal of neuroscience High 27147662
2021 Genetic knockout of Icmt improves survival of HGPS mice and restores vascular smooth muscle cell numbers in the aorta; a pharmacologic ICMT inhibitor (C75) delays senescence and stimulates proliferation of late-passage HGPS cells and Zmpste24-deficient fibroblasts, but does not influence proliferation of wild-type human cells or Zmpste24-deficient cells lacking Icmt, confirming drug specificity for the ICMT pathway. HGPS mouse model with Icmt knockout; synthetic ICMT inhibitor C75; cell proliferation and senescence assays; genetic controls (Zmpste24/Icmt double KO cells) eLife High 33526168
2019 A potent ICMT inhibitor (UCM-1336, compound 3, IC50 = 2 μM) selectively impairs membrane association of all four RAS isoforms, decreases Ras-GTP activity, and inhibits downstream RAS signaling pathways, leading to cell death in Ras-mutated tumor cell lines and improved survival in an in vivo acute myeloid leukemia model. In vitro ICMT enzymatic assay; subcellular fractionation for RAS membrane association; Ras-GTP pull-down; cell viability assays; in vivo AML mouse model Journal of medicinal chemistry Medium 31181882
2007 ICMT inhibition (using AGGC) in pulmonary artery endothelial cells caused redistribution and aggregation of the ER chaperone GRP94, followed by GRP94 protein degradation; these effects were dependent on RhoA activity and caspase activation, indicating that ICMT-dependent RhoA carboxyl methylation is required to maintain GRP94 localization and prevent unfolded protein response-associated apoptosis. ICMT chemical inhibition (AGGC); 2D-PAGE proteomics; immunofluorescence; constitutively active RhoA overexpression rescue; caspase inhibitor American journal of respiratory cell and molecular biology Medium 17347446
2022 PFKFB4 physically interacts with ICMT, promotes ICMT/RAS interaction, controls RAS localization at the plasma membrane, and activates AKT signaling to enhance melanoma cell migration, revealing a glycolysis-independent function of PFKFB4 through ICMT. Co-immunoprecipitation (PFKFB4-ICMT interaction); subcellular localization of RAS; AKT phosphorylation assays; cell migration assays; PFKFB4 knockdown/overexpression Life science alliance Medium 35914811
2019 ICMT inhibition in hepatocellular carcinoma cells suppressed the Ras/Raf/Mek/Erk signaling pathway and inhibited epithelial-mesenchymal transition (EMT), establishing ICMT as mechanistically required for oncogenic Ras signaling and EMT in HCC. ICMT siRNA knockdown and overexpression in HCC cell lines; Western blot for Ras/Raf/Mek/Erk phosphorylation; EMT marker analysis; cell growth and migration assays Biochemical and biophysical research communications Medium 31451223
2019 Wild-type p53 represses ICMT transcription by binding the -209 to -14 region of the ICMT promoter (shown by ChIP assay and promoter truncation/luciferase reporter analysis), while cancer-associated p53 mutants positively regulate ICMT expression through a different promoter region. ChIP assay; ICMT promoter-luciferase reporter constructs; promoter truncation analysis; p53 overexpression/knockdown in cancer cell lines The Journal of biological chemistry Medium 30655292
2011 Prenylcysteine-based ICMT inhibitors (analogs 1a and 1b) exhibit mixed-mode inhibition of human ICMT with the competitive component predominating; cellular treatment with analog 1b alters subcellular localization of GFP-KRas and inhibits both Ras activation and Erk phosphorylation in Jurkat cells. In vitro kinetic inhibition analysis (Ki determination); GFP-KRas subcellular localization by fluorescence microscopy; Ras activation assay; Erk phosphorylation Western blot Bioorganic & medicinal chemistry Medium 22142613
2024 ICMT overexpression enhances invadopodia formation and promotes in vivo lung metastasis; ICMT overexpression also promotes migration and invasion in vitro, suggesting that ICMT acts on substrates regulating the actin cytoskeleton to drive invasive structures. ICMT overexpression in cancer cell lines; invadopodia formation assay; in vivo metastasis mouse model; in vitro migration and invasion assays Biochimie Medium 38301884
2026 ICMT inhibition (genetic and pharmacologic with UCM-1336) reduced INPP5E methylation, displaced INPP5E from membranes, and increased PI(4,5)P2 levels; forced INPP5E membrane targeting partially rescued growth defects caused by ICMT inhibition in BRAFV600E-mutant melanoma cells, identifying INPP5E as an ICMT-dependent substrate mediating BRAFV600E-driven tumor growth. Genetic ICMT knockdown; pharmacologic ICMT inhibition (UCM-1336); INPP5E methylation assay; membrane fractionation; PI(4,5)P2 measurement; forced membrane targeting rescue experiment; xenograft tumor growth assays Proceedings of the National Academy of Sciences of the United States of America High 42127111
2025 RAC1(P29S/C189S), which lacks the C-terminal prenylation site required for ICMT methylation, lost the ability to drive resistance to BRAFV600E inhibitors (vemurafenib/trametinib); combined ICMT inhibition (cysmethynil) with MAPK inhibitors suppressed RAC1(P29S)-driven resistance in vitro and in vivo; mechanistically, combined treatment impaired nuclear translocation of TAZ, whose transcriptional activity accounts for MAPKi resistance downstream of RAC1(P29S). RAC1 prenylation-site mutant (C189S); pharmacologic ICMT inhibition (cysmethynil) combined with MAPK inhibitors; in vitro and in vivo tumor growth assays; TAZ nuclear localization assay; constitutively-active TAZ rescue experiment bioRxivpreprint Medium bio_10.1101_2025.08.10.669587

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf. The Journal of clinical investigation 134 14966563
2013 18F-ICMT-11, a caspase-3-specific PET tracer for apoptosis: biodistribution and radiation dosimetry. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 74 23949910
2002 icmT is essential for pore formation-mediated egress of Legionella pneumophila from mammalian and protozoan cells. Infection and immunity 70 11748165
2011 Mechanism of isoprenylcysteine carboxyl methylation from the crystal structure of the integral membrane methyltransferase ICMT. Molecular cell 46 22195972
2011 Discovery and SAR of methylated tetrahydropyranyl derivatives as inhibitors of isoprenylcysteine carboxyl methyltransferase (ICMT). Journal of medicinal chemistry 41 21661760
2014 Downregulation of microRNA-100 enhances the ICMT-Rac1 signaling and promotes metastasis of hepatocellular carcinoma cells. Oncotarget 39 25361001
2019 A Potent Isoprenylcysteine Carboxylmethyltransferase (ICMT) Inhibitor Improves Survival in Ras-Driven Acute Myeloid Leukemia. Journal of medicinal chemistry 38 31181882
2018 Atomic structure of the eukaryotic intramembrane RAS methyltransferase ICMT. Nature 36 29342140
2018 Clinical translation of [18F]ICMT-11 for measuring chemotherapy-induced caspase 3/7 activation in breast and lung cancer. European journal of nuclear medicine and molecular imaging 32 30259091
2002 The C-terminus of IcmT is essential for pore formation and for intracellular trafficking of Legionella pneumophila within Acanthamoeba polyphaga. Molecular microbiology 31 11918802
2014 Preclinical assessment of carboplatin treatment efficacy in lung cancer by 18F-ICMT-11-positron emission tomography. PloS one 28 24618809
2004 Analysis of the kinetic mechanism of recombinant human isoprenylcysteine carboxylmethyltransferase (Icmt). BMC biochemistry 27 15625008
2021 A small-molecule ICMT inhibitor delays senescence of Hutchinson-Gilford progeria syndrome cells. eLife 23 33526168
2013 Functionalized indoleamines as potent, drug-like inhibitors of isoprenylcysteine carboxyl methyltransferase (Icmt). European journal of medicinal chemistry 23 23514631
2019 ICMT contributes to hepatocellular carcinoma growth, survival, migration and chemoresistance via multiple oncogenic pathways. Biochemical and biophysical research communications 17 31451223
2019 Isoprenylcysteine carboxy methyltransferase (ICMT) is associated with tumor aggressiveness and its expression is controlled by the p53 tumor suppressor. The Journal of biological chemistry 16 30655292
2022 Licoricidin combats gastric cancer by targeting the ICMT/Ras pathway in vitro and in vivo. Frontiers in pharmacology 15 36339587
2007 Inhibition of ICMT induces endothelial cell apoptosis through GRP94. American journal of respiratory cell and molecular biology 15 17347446
2011 Amide-modified prenylcysteine based Icmt inhibitors: Structure-activity relationships, kinetic analysis and cellular characterization. Bioorganic & medicinal chemistry 14 22142613
2005 Structure-function analysis of the C-terminus of IcmT of Legionella pneumophila in pore formation-mediated egress from macrophages. FEMS microbiology letters 12 15621435
2022 PFKFB4 interacts with ICMT and activates RAS/AKT signaling-dependent cell migration in melanoma. Life science alliance 11 35914811
2016 Icmt inhibition exerts anti-angiogenic and anti-hyperpermeability activities impeding malignant pleural effusion. Oncotarget 11 26959120
2014 Mutational analysis of the integral membrane methyltransferase isoprenylcysteine carboxyl methyltransferase (ICMT) reveals potential substrate binding sites. The Journal of biological chemistry 11 25059662
2022 CircRNA hsa_circ_0018289 exerts an oncogenic role in cervical cancer progression through miR-1294/ICMT axis. Journal of clinical laboratory analysis 10 35312113
2006 Genetic and pharmacologic analyses of the role of Icmt in Ras membrane association and function. Methods in enzymology 10 16757321
2021 NRAS is unique among RAS proteins in requiring ICMT for trafficking to the plasma membrane. Life science alliance 9 33579760
2021 Lidocaine exerts anticancer activity in bladder cancer by targeting isoprenylcysteine carboxylmethyltransferase (ICMT). Translational andrology and urology 8 34984187
2016 Deficiency of Isoprenylcysteine Carboxyl Methyltransferase (ICMT) Leads to Progressive Loss of Photoreceptor Function. The Journal of neuroscience : the official journal of the Society for Neuroscience 8 27147662
2020 Development of [18F]ICMT-11 for Imaging Caspase-3/7 Activity during Therapy-Induced Apoptosis. Cancers 7 32781531
2018 Depicting Changes in Tumor Biology in Response to Cetuximab Monotherapy or Combination Therapy by Apoptosis and Proliferation Imaging Using 18F-ICMT-11 and 18F-FLT PET. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 6 29794225
2007 9 Structure and function of isoprenylcysteine carboxylmethyltransferase (Icmt): A key enzyme in CaaX processing. The Enzymes 6 26718043
2013 Mapping peptide thiol accessibility in membranes using a quaternary ammonium isotope-coded mass tag (ICMT). Bioconjugate chemistry 5 23725486
2024 Isoprenylcysteine carboxyl methyltransferase (ICMT) promotes invadopodia formation and metastasis in cancer cells. Biochimie 3 38301884
2018 Use of an Isotope-Coded Mass Tag (ICMT) Method To Determine the Orientation of Cholesterol Oxidase on Model Membranes. Biochemistry 3 30125103
2024 In silico Exploration of a Novel ICMT Inhibitor with More Solubility than Cysmethynil against Membrane Localization of KRAS Mutant in Colorectal Cancer. Current computer-aided drug design 1 38835128
2026 ICMT deficiency ameliorates weight loss and mortality, but not tumor formation in a mouse model of liver cancer. Cell communication and signaling : CCS 0 41808116
2026 Targeting ICMT: A promising strategy in cancer treatment (Review). Oncology letters 0 41877819
2026 ICMT supports BRAFV600E-driven tumor growth by membrane targeting of the CAAX protein INPP5E. Proceedings of the National Academy of Sciences of the United States of America 0 42127111

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