ArticleOncogene2003
Activation of ERK1/2 by deltaRaf-1:ER* represses Bim expression independently of the JNK or PI3K pathways.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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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Who cites it
82 citing papers in PubMed, 172 citations in OpenAlex.
- Antibacterial Activity of Rosmarinic Acid AgainstAnimals : an open access journal from MDPI · 2026Article
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- BCL2 expression is enriched in advanced prostate cancer with features of lineage plasticity.The Journal of clinical investigation · 2024Article
- Advances in the Application of Apoptotic Proteins and Alternative Splicing in Tumor Therapy: A Narrative Review.Iranian journal of public health · 2023Review
- Review
- Manipulation of diacylglycerol and ERK-mediated signaling differentially controls CD8Frontiers in immunology · 2022Article
- Targeting the Intrinsic Apoptosis Pathway: A Window of Opportunity for Prostate Cancer.Cancers · 2021Review
- Therapeutic Potential of Hispidin-Fungal and Plant Polyketide.Journal of fungi (Basel, Switzerland) · 2021Review
- Targeting apoptosis in cancer therapy.Nature reviews. Clinical oncology · 2020Review
- Secretin Prevents Apoptosis in the Developing Cerebellum Through Bcl-2 and Bcl-xL.Journal of molecular neuroscience : MN · 2019Article
- Developing LRP1 Agonists into a Therapeutic Strategy in Acute Myocardial Infarction.International journal of molecular sciences · 2019Review
- RKIP: A Key Regulator in Tumor Metastasis Initiation and Resistance to Apoptosis: Therapeutic Targeting and Impact.Cancers · 2018Review
- Extracellular-Regulated Kinases: Signaling From Ras to ERK Substrates to Control Biological Outcomes.Advances in cancer research · 2018Review
- Exercise-induced circulating extracellular vesicles protect against cardiac ischemia-reperfusion injury.Basic research in cardiology · 2017Article
- Silymarin and its active component silibinin act as novel therapeutic alternatives for salivary gland cancer by targeting the ERK1/2-Bim signaling cascade.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- Activity of distinct growth factor receptor network components in breast tumors uncovers two biologically relevant subtypes.Genome medicine · 2017Article
- Article
- Identification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome.Cellular and molecular life sciences : CMLS · 2016Article
- SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation.Cell cycle (Georgetown, Tex.) · 2016Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
CC139 fibroblasts are one of several model systems in which the Raf --> MEK --> ERK1/2 pathway can inhibit apoptosis independently of the PI3K pathway; however, the precise mechanism for this protective effect is not known. Serum withdrawal from CC139 fibroblasts resulted in the rapid onset of apoptosis, which was prevented by actinomycin D or cycloheximide. Serum withdrawal promoted the rapid, de novo accumulation of Bim(EL), a proapoptotic 'BH3-only' member of the Bcl-2 protein family. Bim(EL) expression was an early event, occurring several hours prior to caspase activation. In contrast to studies in neurons, activation of the JNK --> c-Jun pathway was neither necessary nor sufficient to induce Bim(EL) expression. Selective inhibition of either the ERK pathway (with U0126) or the PI3K pathway (with LY294002) caused an increase in the expression of Bim(EL). Furthermore, selective activation of the ERK1/2 pathway by deltaRaf-1:ER* substantially reduced Bim(EL) expression, abolished conformational changes in Bax and blocked the appearance of apoptotic cells. The ability of deltaRaf-1:ER* to repress Bim(EL) expression required the ERK pathway but was independent of the PI3K --> PDK --> PKB pathway. Thus, serum withdrawal-induced expression of Bim(EL) occurs independently of the JNK --> c-Jun pathway and can be repressed by the ERK pathway independently of the PI3K pathway. This may contribute to Raf- and Ras-induced cell survival at low serum concentrations.
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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.