ArticleThe Journal of clinical investigation2004
Fighting cancer by disrupting C-terminal methylation of signaling proteins.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice.Experimental neurology · 2024Article
- Review
- Role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury.Ageing research reviews · 2023Review
- Small-Molecule RAS Inhibitors as Anticancer Agents: Discovery, Development, and Mechanistic Studies.International journal of molecular sciences · 2022Review
- Homocysteine-methionine cycle is a metabolic sensor system controlling methylation-regulated pathological signaling.Redox biology · 2020Article
- Regulation of the Ras-Related Signaling Pathway by Small Molecules Containing an Indole Core Scaffold: A Potential Antitumor Therapy.Frontiers in pharmacology · 2020Review
- Isoprenyl carboxyl methyltransferase inhibitors: a brief review including recent patents.Amino acids · 2017Review
- Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins.ISRN oncology · 2013Review
- Role of isoprenylcysteine carboxylmethyltransferase-catalyzed methylation in Rho function and migration.The Journal of biological chemistry · 2009Article
- Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer.Oncogene · 2007Review
- The isoprenoid substrate specificity of isoprenylcysteine carboxylmethyltransferase: development of novel inhibitors.The Journal of biological chemistry · 2005Article
- A small-molecule inhibitor of isoprenylcysteine carboxyl methyltransferase with antitumor activity in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Analysis of the kinetic mechanism of recombinant human isoprenylcysteine carboxylmethyltransferase (Icmt).BMC biochemistry · 2004Article
- RHO methylation matters: a role for isoprenylcysteine carboxylmethyltransferase in cell migration and adhesion.Cell adhesion & migrationArticle
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Protein methylation at the C-terminus of mammalian isoprenylated proteins has been implicated in membrane attachment, protein-protein interactions, and protein stability. A new paper describes surprising results: in the absence of methylation some target proteins have increased stability, whereas others have decreased stability. The decreased stability of the RhoA protein is correlated with an increased resistance to Ras-dependent transformation and suggests the basis for the development of a new approach to antitumor therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.