ReviewJournal of molecular medicine (Berlin, Germany)2016
K-Ras protein as a drug target.
Review in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 101 citations in OpenAlex.
- Brønsted-basic small molecules activate GTP hydrolysis in KRAS-Q61 mutants.Nature chemical biology · 2026Article
- AGAP1 and noncanonical GDP binding regulate triple-negative breast cancer development.Cellular and molecular life sciences : CMLS · 2026Article
- The Role of Gonadotropins and Growth Factor in Regulating Ras During Maturation in Cumulus-Oocyte Complexes of Pigs.Animals : an open access journal from MDPI · 2025Article
- The Persistent Power of the Taxane/Platin Chemotherapy.Cancers · 2025Review
- Review
- Sotorasib resistance triggers epithelial-mesenchymal transition and activates AKT and P38-mediated signaling.Frontiers in molecular biosciences · 2025Article
- KRas4b-Calmodulin Interaction with Membrane Surfaces: Role of Headgroup, Acyl Chain, and Electrostatics.Biochemistry · 2024Article
- KRAS G12C mutation in NSCLC in a small genetic center: insights into sotorasib therapy response potential.Scientific reports · 2024Article
- The impact of histone lactylation on the tumor microenvironment and metabolic pathways and its potential in cancer therapy.Genes & genomics · 2024Review
- Transglutaminase 2 serves as a pathogenic hub gene of KRAS mutant colon cancer based on integrated analysis.World journal of gastrointestinal oncology · 2024Article
- Mutant KRAS-activated circATXN7 fosters tumor immunoescape by sensitizing tumor-specific T cells to activation-induced cell death.Nature communications · 2024Article
- Ras interacting protein 1 facilitated proliferation and invasion of diffuse large B-cell lymphoma cells.Cancer biology & therapy · 2023Article
- A new ferrocene derivative blocks K-Ras localization and function by oxidative modification at His95.Life science alliance · 2023Article
- Polarization of Cancer-Associated Macrophages Maneuver Neoplastic Attributes of Pancreatic Ductal Adenocarcinoma.Cancers · 2023Review
- Case Report: Long-term survival of a patient with advanced rectal cancer and multiple pelvic recurrences after seven surgeries.Frontiers in oncology · 2023Article
- Peptidomimetics designed to bind to RAS effector domain are promising cancer therapeutic compounds.Scientific reports · 2022Article
- KRAS: A Druggable Target in Colon Cancer Patients.International journal of molecular sciences · 2022Review
- Machine learning-driven multiscale modeling reveals lipid-dependent dynamics of RAS signaling proteins.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Characterization of KRAS Mutation Subtypes in Non-small Cell Lung Cancer.Molecular cancer therapeutics · 2021Article
- KRAS4A induces metastatic lung adenocarcinomas in vivo in the absence of the KRAS4B isoform.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
K-Ras proteins are major drivers of human cancers, playing a direct causal role in about one million cancer cases/year. In cancers driven by mutant K-Ras, the protein is locked in the active, GTP-bound state constitutively, through a defect in the off-switch mechanism. As such, the mutant protein resembles the normal K-Ras protein from a structural perspective, making therapeutic attack extremely challenging. K-Ras is a member of a large family of related proteins, which share very similar GDP/GTP-binding domains, making specific therapies more difficult. Furthermore, Ras proteins lack pockets to which small molecules can bind with high affinity, with a few interesting exceptions. However, new insights into the structure and function of K-Ras proteins reveal opportunities for intervention that were not appreciated many years ago, when efforts were launched to develop K-Ras therapies. Furthermore, K-Ras undergoes post-translational modification and interactions with cellular signaling proteins that present additional therapeutic opportunities, such as specific binding to calmodulin and regulation of non-canonical Wnt signaling.
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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.