ReviewNature reviews. Molecular cell biology2011
Regulating the regulator: post-translational modification of RAS.
Review in Nature reviews. Molecular cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 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
326 citing papers in PubMed, 542 citations in OpenAlex.
- Farnesyltransferase Enables Modular Assembly of Dual-Functional Nanobody Conjugates for in Vivo Imaging of Inflammation.Angewandte Chemie (International ed. in English) · 2026Article
- Regulation of Membrane Association and Downstream Effector Interaction of K-Ras by Its Hypervariable Region.Membranes · 2026Article
- High yield production of C-terminally processed KRAS4a, HRAS, and NRAS for biophysical study.Protein expression and purification · 2026Article
- RAS-PI3Kα signaling regulates KrasG12D-induced lymphangiogenesis in complex lymphatic anomalies.Disease models & mechanisms · 2026Article
- Combinatorial post-translational modification reprogramming of the endomembrane system in colorectal cancer.Translational cancer research · 2026Article
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.Research square · 2026Article
- The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation.Oncotarget · 2026Article
- Temperature and lipid composition differentially regulate KRAS assemblies on membranes.Chemical communications (Cambridge, England) · 2026Article
- Mechanistic insights on spatiotemporal control of Ras-signaling.Biological chemistry · 2026Review
- Revisiting RAS family GTPase signaling: effector selectivity and oncogenic bypass.The Biochemical journal · 2026Review
- Sensing and Reprogramming Surface Receptor Activation With Synthetic Transcriptional Circuits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.bioRxiv : the preprint server for biology · 2026Article
- Bioorthogonal Click Chemistry for Antibody-Free Profiling of Acetylation, Propionylation, and Butyrylation inACS infectious diseases · 2026Article
- Allostery in Biomolecular Condensates.Journal of molecular biology · 2026Review
- KRAS Inhibition in Pancreatic Ductal Adenocarcinoma.Journal of clinical medicine · 2026Review
- Melanoma: Pathogenesis and Targeted Therapy.MedComm · 2026Review
- Palmitoylation reprograms the intestinal mucosal barrier microenvironment: potential mechanisms and promising therapeutic targets.Frontiers in pharmacology · 2026Review
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Helical sensors of membrane saturation: Changes in orientation and curvature preference.Biophysical journal · 2025Article
- Proteomic Perspectives on KRAS-Driven Cancers and Emerging Therapeutic Approaches.Current oncology (Toronto, Ont.) · 2025Review
266 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
RAS proteins are monomeric GTPases that act as binary molecular switches to regulate a wide range of cellular processes. The exchange of GTP for GDP on RAS is regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs), which regulate the activation state of RAS without covalently modifying it. By contrast, post-translational modifications (PTMs) of RAS proteins direct them to various cellular membranes and, in some cases, modulate GTP-GDP exchange. Important RAS PTMs include the constitutive and irreversible remodelling of its carboxy-terminal CAAX motif by farnesylation, proteolysis and methylation, reversible palmitoylation, and conditional modifications, including phosphorylation, peptidyl-prolyl isomerisation, monoubiquitylation, diubiquitylation, nitrosylation, ADP ribosylation and glucosylation.
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.