ArticleMolecular and cellular biology2008
Survival signaling by C-RAF: mitochondrial reactive oxygen species and Ca2+ are critical targets.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells.Molecular oncology · 2026Article
- Mitochondrial CLPB is a pro-survival factor at the onset of granulocytic differentiation of mouse myeloblastic cells.Apoptosis : an international journal on programmed cell death · 2025Article
- Modulation of Innate Immune Memory Dynamics by Subcellular Reactive Oxygen Species.Antioxidants & redox signaling · 2023Review
- miR-7-5p Antagomir Protects Against Inflammation-Mediated Apoptosis and Lung Injury via Targeting Raf-1 In Vitro and In Vivo.Inflammation · 2023Article
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- Research of Mitochondrial Function, Structure, Dynamics and Intracellular Organization.International journal of molecular sciences · 2023Article
- The Complex Interplay between Mitochondria, ROS and Entire Cellular Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- The Synergistic Cytotoxic Effects of GW5074 and Sorafenib by Impacting Mitochondrial Functions in Human Colorectal Cancer Cell Lines.Frontiers in oncology · 2022Article
- Dependence of PINK1 accumulation on mitochondrial redox system.Aging cell · 2020Article
- Article
- The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2019Review
- The oxidoreductase p66Shc acts as tumor suppressor in BRAFV600E-transformed cells.Molecular oncology · 2018Article
- Calcium oxalate crystals induces tight junction disruption in distal renal tubular epithelial cells by activating ROS/Akt/p38 MAPK signaling pathway.Renal failure · 2017Article
- Synchronism in mitochondrial ROS flashes, membrane depolarization and calcium sparks in human carcinoma cells.Biochimica et biophysica acta. Bioenergetics · 2017Article
- Novel Insights into the PKCβ-dependent Regulation of the Oxidoreductase p66Shc.The Journal of biological chemistry · 2016Article
- cJun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation.Scientific reports · 2016Article
- Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC Cells.Oxidative medicine and cellular longevity · 2016Article
- The regulation of coenzyme q biosynthesis in eukaryotic cells: all that yeast can tell us.Molecular syndromology · 2014Article
- A p38MAPK/MK2 signaling pathway leading to redox stress, cell death and ischemia/reperfusion injury.Cell communication and signaling : CCS · 2014Article
- RAF and antioxidants prevent cell death induction after growth factor abrogation through regulation of Bcl-2 proteins.Experimental cell research · 2013Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Survival signaling by RAF occurs through largely unknown mechanisms. Here we provide evidence for the first time that RAF controls cell survival by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and Ca(2+). Interleukin-3 (IL-3) withdrawal from 32D cells resulted in ROS production, which was suppressed by activated C-RAF. Oncogenic C-RAF decreased the percentage of apoptotic cells following treatment with staurosporine or the oxidative stress-inducing agent tert-butyl hydroperoxide. However, it was also the case that in parental 32D cells growing in the presence of IL-3, inhibition of RAF signaling resulted in elevated mitochondrial ROS and Ca(2+) levels. Cell death is preceded by a ROS-dependent increase in mitochondrial Ca(2+), which was absent from cells expressing transforming C-RAF. Prevention of mitochondrial Ca(2+) overload after IL-3 deprivation increased cell viability. MEK was essential for the mitochondrial effects of RAF. In summary, our data show that survival control by C-RAF involves controlling ROS production, which otherwise perturbs mitochondrial Ca(2+) homeostasis.
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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.