ArticleMolecular and cellular biology2004
The molecular scaffold KSR1 regulates the proliferative and oncogenic potential of cells.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 150 citations in OpenAlex.
- HRAS promotes mutant NRAS-driven transformation with codon and allele specificity.Science signaling · 2026Article
- Dual RAF inhibition outperforms RAF-MEK combinations for suppressing ERK signaling in KRAS mutant cells.NPJ systems biology and applications · 2026Article
- Endothelial KSR2 regulated by genetic variation protects against atherosclerosis through AMPKα1 stabilization.Theranostics · 2026Article
- Diagnostic and prognostic biomarkers associated with histotype in advanced epithelial ovarian cancer.Scientific reports · 2025Article
- Targeting Kinase Suppressor of Ras 1 (KSR1) for Cancer Therapy.Pharmaceutics · 2025Review
- Wild-type RAS signaling is an essential therapeutic target inScience signaling · 2025Article
- KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance.Molecular cancer research : MCR · 2025Article
- LINC02167 stabilizes KSR1 mRNA in an mJournal of experimental & clinical cancer research : CR · 2025Article
- PRUNE1 and NME/NDPK family proteins influence energy metabolism and signaling in cancer metastases.Cancer metastasis reviews · 2024Review
- A guide to ERK dynamics, part 1: mechanisms and models.The Biochemical journal · 2023Article
- SOS1 and KSR1 modulate MEK inhibitor responsiveness to target resistant cell populations based on PI3K and KRAS mutation status.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Kinase Suppressor of RAS 1 (KSR1) Maintains the Transformed Phenotype of BRAFV600E Mutant Human Melanoma Cells.International journal of molecular sciences · 2023Article
- KSR induces RAS-independent MAPK pathway activation and modulates the efficacy of KRAS inhibitors.Molecular oncology · 2022Article
- KSR2-14-3-3ζ complex serves as a biomarker and potential therapeutic target in sorafenib-resistant hepatocellular carcinoma.Biomarker research · 2022Article
- KSR1- and ERK-dependent translational regulation of the epithelial-to-mesenchymal transition.eLife · 2021Article
- BRAP2 inhibits the Ras/Raf/MEK and PI3K/Akt pathways in leukemia cells, thereby inducing apoptosis and inhibiting cell growth.Experimental and therapeutic medicine · 2021Article
- Effects of CXCL12 isoforms in a pancreatic pre-tumour cellular model: Microarray analysis.World journal of gastroenterology · 2021Article
- Ras Mitogen-activated Protein Kinase Signaling and Kinase Suppressor of Ras as Therapeutic Targets for Hepatocellular Carcinoma.Journal of liver cancer · 2021Review
- A Gene Expression High-Throughput Screen (GE-HTS) for Coordinated Detection of Functionally Similar Effectors in Cancer.Cancers · 2020Review
- RIAM-VASP Module Relays Integrin Complement Receptors in Outside-In Signaling Driving Particle Engulfment.Cells · 2020Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The specificity of signaling through mitogen-activated protein kinase pathways has been attributed to both the control of intensity and duration of signaling and the actions of protein scaffolds. Here we demonstrate that the molecular scaffold KSR1 regulates the intensity and duration of ERK activation to modulate a cell's proliferative and oncogenic potential. Deletion of KSR1 eliminates the prolonged phase of ERK activation induced by platelet-derived growth factor and blocks Ras(V12)-induced transformation. The introduction of KSR1 into KSR1(-/-) mouse embryo fibroblasts causes a concentration-dependent increase in signaling and transformation, to a maximum at 14 times the wild-type KSR1 expression levels, but inhibits these responses at higher expression levels. An increase in KSR1 expression to levels that are optimal for signaling leads to a threefold increase in proliferative capacity and is coincident with the level of KSR1 expression that maximally associates with all members of the Raf/MEK/ERK cascade. These data reveal that cells contain a reserve proliferative capacity that is accessible by the optimal expression of a noncatalytic signaling component and that altering the expression level of a molecular scaffold can modulate the actions of growth factors and oncogenes.
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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.