ArticleMolecular and cellular biology2014
Caveolin-1 is required for kinase suppressor of Ras 1 (KSR1)-mediated extracellular signal-regulated kinase 1/2 activation, H-RasV12-induced senescence, and transformation.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Differential Radiomodulatory Effects of Sodium Aminodihydrophthalazinedione (TameronInternational journal of molecular sciences · 2026Article
- A guide to ERK dynamics, part 1: mechanisms and models.The Biochemical journal · 2023Article
- Kinase Suppressor of RAS 1 (KSR1) Maintains the Transformed Phenotype of BRAFV600E Mutant Human Melanoma Cells.International journal of molecular sciences · 2023Article
- iTRAQ proteomics of sentinel lymph nodes for identification of extracellular matrix proteins to flag metastasis in early breast cancer.Scientific reports · 2022Article
- Molecular dissection on inhibition of Ras-induced cellular senescence by small t antigen of SV40.Cellular and molecular life sciences : CMLS · 2022Article
- N6-methyladenosine demethylase FTO promotes growth and metastasis of gastric cancer via mCell death & disease · 2022Article
- Role of thyroid hormone-integrin αvβ3-signal and therapeutic strategies in colorectal cancers.Journal of biomedical science · 2021Review
- Caveolin-1 downregulation promotes the dopaminergic neuron-like differentiation of human adipose-derived mesenchymal stem cells.Neural regeneration research · 2021Article
- Ras Mitogen-activated Protein Kinase Signaling and Kinase Suppressor of Ras as Therapeutic Targets for Hepatocellular Carcinoma.Journal of liver cancer · 2021Review
- Caveolin-1, a master regulator of cellular senescence.Cancer metastasis reviews · 2020Review
- lncRNA ANRIL Ameliorates Oxygen and Glucose Deprivation (OGD) Induced Injury in Neuron Cells via miR-199a-5p/CAV-1 Axis.Neurochemical research · 2020Article
- Metformin Inhibits Propofol-Induced Apoptosis of Mouse Hippocampal Neurons HT-22 Through Downregulating Cav-1.Drug design, development and therapy · 2020Article
- Inhaled gold nanoparticles cause cerebral edema and upregulate endothelial aquaporin 1 expression, involving caveolin 1 dependent repression of extracellular regulated protein kinase activity.Particle and fibre toxicology · 2019Article
- Simvastatin delays castration‑resistant prostate cancer metastasis and androgen receptor antagonist resistance by regulating the expression of caveolin‑1.International journal of oncology · 2019Article
- Caveolin‑1 regulates oxidative stress‑induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro.Molecular medicine reports · 2017Article
- Bidirectional alteration of Cav-1 expression is associated with mitogenic conversion of its function in gastric tumor progression.BMC cancer · 2017Article
- KSR as a therapeutic target for Ras-dependent cancers.Expert opinion on therapeutic targets · 2017Review
- Coordinating ERK signaling via the molecular scaffold Kinase Suppressor of Ras.F1000Research · 2017Review
- Design, Assessment, and in vivo Evaluation of a Computational Model Illustrating the Role of CAV1 in CD4(+) T-lymphocytes.Frontiers in immunology · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The molecular scaffold kinase suppressor of Ras 1 (KSR1) regulates the activation of the Raf/MEK/extracellular signal-regulated kinase (ERK) signal transduction pathway. KSR1 disruption in mouse embryo fibroblasts (MEFs) abrogates growth factor-induced ERK activation, H-Ras(V12)-induced replicative senescence, and H-Ras(V12)-induced transformation. Caveolin-1 has been primarily described as a major component of the coating structure of caveolae, which can serve as a lipid binding adaptor protein and coordinates the assembly of Ras, Raf, MEK, and ERK. In this study, we show that KSR1 interacts with caveolin-1 and is responsible for MEK and ERK redistribution to caveolin-1-rich fractions. The interaction between KSR1 and caveolin-1 is essential for optimal activation of ERK as a KSR1 mutant unable to interact with caveolin-1 does not efficiently mediate growth factor-induced ERK activation at the early stages of pathway activation. Furthermore, abolishing the KSR1-caveolin-1 interaction increases growth factor demands to promote H-Ras(V12)-induced proliferation and has adverse effects on H-Ras(V12)-induced cellular senescence and transformation. These data show that caveolin-1 is necessary for optimal KSR1-dependent ERK activation by growth factors and oncogenic Ras.
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