ArticleFrontiers in oncology2012
Crosstalk between Bcl-2 family and Ras family small GTPases: potential cell fate regulation?
Article in Frontiers in oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 25 citations in OpenAlex.
- Multi-sampling allows intra-tumoral heterogeneity querying and vulnerability profiling in glioblastoma.Neuro-oncology · 2026Article
- Bcl-2 dependent modulation of Hippo pathway in cancer cells.Cell communication and signaling : CCS · 2024Article
- In-depth analysis of the interplay between oncogenic mutations and NK cell-mediated cancer surveillance in solid tumors.Oncoimmunology · 2024Review
- PTPσ inhibitors promote hematopoietic stem cell regeneration.Nature communications · 2019Article
- Perspectives of RAS and RHEB GTPase Signaling Pathways in Regenerating Brain Neurons.International journal of molecular sciences · 2018Review
- Subcellular Distribution of S-Nitrosylated H-Ras in Differentiated and Undifferentiated PC12 Cells during Hypoxia.Cell journal · 2017Article
- Inferring gene and protein interactions using PubMed citations and consensus Bayesian networks.PloS one · 2017Article
- Antitumor effects of minodronate, a third-generation nitrogen-containing bisphosphonate, in synergy with γδT cells in human glioblastoma in vitro and in vivo.Journal of neuro-oncology · 2016Article
- The Tumor-suppressive Small GTPase DiRas1 Binds the Noncanonical Guanine Nucleotide Exchange Factor SmgGDS and Antagonizes SmgGDS Interactions with Oncogenic Small GTPases.The Journal of biological chemistry · 2016Article
- Mitochondrial Proteins (e.g., VDAC, Bcl-2, HK, ANT) as Major Control Points in Oncology.Frontiers in oncology · 2014Article
- The mitochondrial permeability transition pore and cancer: molecular mechanisms involved in cell death.Frontiers in oncology · 2014Review
- Protect and serve: Bcl-2 proteins as guardians and rulers of cancer cell survival.Cell cycle (Georgetown, Tex.) · 2013Article
- Ras and rheb signaling in survival and cell death.Cancers · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell fate regulation is a function of diverse cell signaling pathways that promote cell survival and or inhibit cell death execution. In this regard, the role of the Bcl-2 family in maintaining a tight balance between cell death and cell proliferation has been extensively studied. The conventional dogma links cell fate regulation by the Bcl-2 family to its effect on mitochondrial permeabilization and apoptosis amplification. However, recent evidence provide a novel mechanism for death regulation by the Bcl-2 family via modulating cellular redox metabolism. For example overexpression of Bcl-2 has been shown to contribute to a pro-oxidant intracellular milieu and down-regulation of cellular superoxide levels enhanced death sensitivity of Bcl-2 overexpressing cells. Interestingly, gene knockdown of the small GTPase Rac1 or pharmacological inhibition of its activity also reverted death phenotype in Bcl-2 expressing cells. This appears to be a function of an interaction between Bcl-2 and Rac1. Similar functional associations have been described between the Bcl-2 family and other members of the Ras superfamily. These interactions at the mitochondria provide novel opportunities for strategic therapeutic targeting of drug-resistant cancers.
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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.