ArticleMolecular biology of the cell2019
Isoform-specific Ras signaling is growth factor dependent.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer.EMBO reports · 2026Article
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- Quantitative modeling of signaling in aggressive B cell lymphoma unveils conserved core network.PLoS computational biology · 2024Article
- Modeling unveils sex differences of signaling networks in mouse embryonic stem cells.Molecular systems biology · 2023Article
- kboolnet: a toolkit for the verification, validation, and visualization of reaction-contingency (rxncon) models.BMC bioinformatics · 2023Article
- Dynamic regulation of RAS and RAS signaling.The Biochemical journal · 2023Article
- Editorial: Identifying the isoform-specific roles of RAS paralogs in health and disease.Frontiers in cell and developmental biology · 2023Article
- Computational Random Mutagenesis to Investigate RAS Mutant Signaling.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Dissecting the clinicopathologic, genomic, and immunophenotypic correlates of KRASAnnals of oncology : official journal of the European Society for Medical Oncology · 2022Article
- Peptidomimetics designed to bind to RAS effector domain are promising cancer therapeutic compounds.Scientific reports · 2022Article
- Differential roles and regulation of the protein kinases PAK4, PAK5 and PAK6 in melanoma cells.The Biochemical journal · 2022Article
- Article
- Comparative Analysis and Isoform-Specific Therapeutic Vulnerabilities of KRAS Mutations in Non-Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach.Cell reports · 2021Article
- Neuroblastoma signalling models unveil combination therapies targeting feedback-mediated resistance.PLoS computational biology · 2021Article
- EGFR-RAS-MAPK signaling is confined to the plasma membrane and associated endorecycling protrusions.The Journal of cell biology · 2021Article
- Ras Variant Biology and Contributions to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021Review
- K-Ras prenylation as a potential anticancer target.Cancer metastasis reviews · 2020Review
- Therapeutic targeting of RAS: New hope for drugging the "undruggable".Biochimica et biophysica acta. Molecular cell research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
HRAS, NRAS, and KRAS isoforms are almost identical proteins that are ubiquitously expressed and activate a common set of effectors. In vivo studies have revealed that they are not biologically redundant; however, the isoform specificity of Ras signaling remains poorly understood. Using a novel panel of isogenic SW48 cell lines endogenously expressing wild-type or G12V-mutated activated Ras isoforms, we have performed a detailed characterization of endogenous isoform-specific mutant Ras signaling. We find that despite displaying significant Ras activation, the downstream outputs of oncogenic Ras mutants are minimal in the absence of growth factor inputs. The lack of mutant KRAS-induced effector activation observed in SW48 cells appears to be representative of a broad panel of colon cancer cell lines harboring mutant KRAS. For MAP kinase pathway activation in KRAS-mutant cells, the requirement for coincident growth factor stimulation occurs at an early point in the Raf activation cycle. Finally, we find that Ras isoform-specific signaling was highly context dependent and did not conform to the dogma derived from ectopic expression studies.
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.