ArticleNature communications2014
Decreased tumorigenesis in mice with a Kras point mutation at C118.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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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
12 citing papers in PubMed, 22 citations in OpenAlex.
- Oncogenic mutant KRAS inhibition through oxidation at cysteine 118.Molecular oncology · 2025Article
- Detection of differential bait proteoforms through immunoprecipitation-mass spectrometry data analysis.Scientific data · 2024Article
- A multienzyme S-nitrosylation cascade regulates cholesterol homeostasis.Cell reports · 2022Article
- CCDC65, a Gene Knockout that leads to Early Death of Mice, acts as a potentially Novel Tumor Suppressor in Lung Adenocarcinoma.International journal of biological sciences · 2022Article
- ROS regulation of RAS and vulva development in Caenorhabditis elegans.PLoS genetics · 2020Article
- Capturing the primordial Kras mutation initiating urethane carcinogenesis.Nature communications · 2020Article
- Biology, pathology, and therapeutic targeting of RAS.Advances in cancer research · 2020Review
- Cysteine-based regulation of redox-sensitive Ras small GTPases.Redox biology · 2019Review
- A model for RAS mutation patterns in cancers: finding the sweet spot.Nature reviews. Cancer · 2018Review
- Somatic Mutations in Prostate Cancer: Closer to Personalized Medicine.Molecular diagnosis & therapy · 2017Review
- Biochemical Classification of Disease-associated Mutants of RAS-like Protein Expressed in Many Tissues (RIT1).The Journal of biological chemistry · 2016Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
KRAS, NRAS or HRAS genes are mutated to encode an active oncogenic protein in a quarter of human cancers. Redox-dependent reactions can also lead to Ras activation in a manner dependent upon the thiol residue of cysteine 118 (C118). Here, to investigate the effect of mutating this residue on tumorigenesis, we introduce a C118S mutation into the endogenous murine Kras allele and expose the resultant mice to the carcinogen urethane, which induces Kras mutation-positive lung tumours. We report that Kras(+/C118S) and Kras(C118S/C118S) mice develop fewer lung tumours. Although the Kras(C118S) allele does not appear to affect tumorigenesis when the remaining Kras allele is conditionally oncogenic, there is a moderate imbalance of oncogenic mutations favouring the native Kras allele in tumours from Kras(+/C118S) mice treated with urethane. We conclude that the Kras(C118S) allele impedes urethane-induced lung tumorigenesis.
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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.