ArticleBlood2008
Inactivating Icmt ameliorates K-RAS-induced myeloproliferative disease.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 89 citations in OpenAlex.
- ICMT supports BRAFProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting ICMT: A promising strategy in cancer treatment (Review).Oncology letters · 2026Review
- ICMT deficiency ameliorates weight loss and mortality, but not tumor formation in a mouse model of liver cancer.Cell communication and signaling : CCS · 2026Article
- Protein Prenyltransferases and Their Inhibitors: Structural and Functional Characterization.International journal of molecular sciences · 2022Review
- Licoricidin combats gastric cancer by targeting the ICMT/Ras pathway in vitro and in vivo.Frontiers in pharmacology · 2022Article
- Suppression of isoprenylcysteine carboxylmethyltransferase compromises DNA damage repair.Life science alliance · 2021Article
- Toward a New Therapy for Rapidly Aging Children.ACS central science · 2021Article
- Ras Isoforms from Lab Benches to Lives-What Are We Missing and How Far Are We?International journal of molecular sciences · 2021Review
- NRAS is unique among RAS proteins in requiring ICMT for trafficking to the plasma membrane.Life science alliance · 2021Article
- A small-molecule ICMT inhibitor delays senescence of Hutchinson-Gilford progeria syndrome cells.eLife · 2021Article
- NMR in integrated biophysical drug discovery for RAS: past, present, and future.Journal of biomolecular NMR · 2020Review
- Small change, big effect: Taking RAS by the tail through suppression of post-prenylation carboxylmethylation.Small GTPases · 2020Review
- TargetingInternational journal of molecular sciences · 2020Review
- Article
- Review
- Biology, pathology, and therapeutic targeting of RAS.Advances in cancer research · 2020Review
- Beyond the Mevalonate Pathway: Control of Post-Prenylation Processing by Mutant p53.Frontiers in oncology · 2020Review
- From basic researches to new achievements in therapeutic strategies of KRAS-driven cancers.Cancer biology & medicine · 2019Article
- Isoprenylcysteine carboxy methyltransferase (ICMT) is associated with tumor aggressiveness and its expression is controlled by the p53 tumor suppressor.The Journal of biological chemistry · 2019Article
- Posttranslational Modifications of RAS Proteins.Cold Spring Harbor perspectives in medicine · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Hyperactive signaling through the RAS proteins is involved in the pathogenesis of many forms of cancer. The RAS proteins and many other intracellular signaling proteins are either farnesylated or geranylgeranylated at a carboxyl-terminal cysteine. That isoprenylcysteine is then carboxyl methylated by isoprenylcysteine carboxyl methyltransferase (ICMT). We previously showed that inactivation of Icmt mislocalizes the RAS proteins away from the plasma membrane and blocks RAS transformation of mouse fibroblasts, suggesting that ICMT could be a therapeutic target. However, nothing is known about the impact of inhibiting ICMT on the development of malignancies in vivo. In the current study, we tested the hypothesis that inactivation of Icmt would inhibit the development or progression of a K-RAS-induced myeloproliferative disease in mice. We found that inactivating Icmt reduced splenomegaly, the number of immature myeloid cells in peripheral blood, and tissue infiltration by myeloid cells. Moreover, in the absence of Icmt, the ability of K-RAS-expressing hematopoietic cells to form colonies in methylcellulose without exogenous growth factors was reduced dramatically. Finally, inactivating Icmt reduced lung tumor development and myeloproliferation phenotypes in a mouse model of K-RAS-induced cancer. We conclude that inactivation of Icmt ameliorates phenotypes of K-RAS-induced malignancies in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.