ArticleBMC cell biology2002
Negative regulation of mitochondrial VDAC channels by C-Raf kinase.
Article in BMC cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 64 citations in OpenAlex.
- HIPK3 Inhibition by Exosomal hsa-miR-101-3p Is Related to Metabolic Reprogramming in Colorectal Cancer.Frontiers in oncology · 2021Article
- VDACs: An Outlook on Biochemical Regulation and Function in Animal and Plant Systems.Frontiers in physiology · 2021Review
- Gold/alpha-lactalbumin nanoprobes for the imaging and treatment of breast cancer.Nature biomedical engineering · 2020Article
- Review
- The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2019Review
- Mechanism of translation control of the alternative Drosophila melanogaster Voltage Dependent Anion-selective Channel 1 mRNAs.Scientific reports · 2018Article
- Voltage-Dependent Anion Channel 1 As an Emerging Drug Target for Novel Anti-Cancer Therapeutics.Frontiers in oncology · 2017Review
- Signaling to cardiac hypertrophy: insights from human and mouse RASopathies.Molecular medicine (Cambridge, Mass.) · 2012Review
- VDAC1: from structure to cancer therapy.Frontiers in oncology · 2012Article
- Raf family kinases: old dogs have learned new tricks.Genes & cancer · 2011Article
- Ras homolog enriched in brain (Rheb) enhances apoptotic signaling.The Journal of biological chemistry · 2010Article
- Identification of novel in vivo phosphorylation sites of the human proapoptotic protein BAD: pore-forming activity of BAD is regulated by phosphorylation.The Journal of biological chemistry · 2009Article
- Article
- Regulation of hexokinase binding to VDAC.Journal of bioenergetics and biomembranes · 2008Review
- Survival signaling by C-RAF: mitochondrial reactive oxygen species and Ca2+ are critical targets.Molecular and cellular biology · 2008Article
- Mitogen-activated protein kinases in heart development and diseases.Circulation · 2007Review
- Apoptosis of hematopoietic cells induced by growth factor withdrawal is associated with caspase-9 mediated cleavage of Raf-1.Oncogene · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrowth of cancer cells results from the disturbance of positive and negative growth control mechanisms and the prolonged survival of these genetically altered cells due to the failure of cellular suicide programs. Genetic and biochemical approaches have identified Raf family serine/threonine kinases B-Raf and C-Raf as major mediators of cell survival. C-Raf cooperates with Bcl-2/Bcl-XL in suppression of apoptosis by a mechanism that involves targeting of C-Raf to the outer mitochondrial membrane and inactivation of the pro-apoptotic protein Bad. However, apoptosis suppression by C-Raf also occurs in cells lacking expression of Bad or Bcl-2.
resultsHere we show that even in the absence of Bcl-2/Bcl-XL, mitochondria-targeted C-Raf inhibits cytochrome c release and caspase activation induced by growth factor withdrawal. To clarify the mechanism of Bcl-2 independent survival control by C-Raf at the mitochondria a search for novel mitochondrial targets was undertaken that identified voltage-dependent anion channel (VDAC), a mitochondrial protein (porin) involved in exchange of metabolites for oxidative phosphorylation. C-Raf forms a complex with VDAC in vivo and blocks reconstitution of VDAC channels in planar bilayer membranes in vitro.
conclusionWe propose that this interaction may be responsible for the Raf-induced inhibition of cytochrome c release from mitochondria in growth factor starved cells. Moreover, C-Raf kinase-induced VDAC inhibition may regulate the metabolic function of mitochondria and mediate the switch to aerobic glycolysis that is common to cancer cells.
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.