ReviewTrends in biochemical sciences2011
The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation.
Review in Trends in biochemical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,014 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
1,014 citing papers in PubMed.
- Host andGut microbes · 2026Article
- Aberrant sialylation in cancer: From molecular mechanisms to potential therapeutics.Genes & diseases · 2026Review
- Excessive activation of the RAS/MAPK pathway triggers adult-onset motor axonal degeneration.iScience · 2026Article
- Targeting the PI3K/Akt Signaling Pathway: A Promising Therapeutic Strategy to Reduce Cancer Mortality and Overcome Chemoresistance.Health science reports · 2026Article
- 4H-CRCXL Mitigates RasV12-Induced Phenotypes in Glioblastoma Model of Drosophila.Molecular carcinogenesis · 2026Article
- Upstream regulatory mechanisms and clinical significance of IQGAP2 deficiency in affecting PI3K activity to drive cell proliferation.Human cell · 2026Article
- Review
- Therapeutic Resistance in Melanoma: Molecular Mechanisms and Emerging Pharmaceutical Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- IGF2 knockout reduces but does not abolish osteosarcoma growth in vitro and in vivo.FEBS open bio · 2026Article
- GPCR-Driven Muscarinic M1 and Histamine H1 Receptor Signaling Converging on the PI3K/Akt/mTOR Pathway: Functional Integration in Neuroinflammation and Myelin Repair in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Lipid nanoparticles as active biointerfaces: From membrane interaction to systemic dysregulation.Acta pharmaceutica Sinica. B · 2026Review
- PIK3CA silencing restores anoikis sensitivity in endothelial cells.Molecular biology reports · 2026Article
- A structure-based modeling approach identifies effective drug combinations for RAS-mutant acute myeloid leukemia.iScience · 2026Article
- Selenium Nanoparticles Selectively Target KRAS G13D to Inhibit Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ovarian toxic effects of micro- and nanoplastics (Review).Experimental and therapeutic medicine · 2026Review
- PCOS Serum Promotes Endometrial Cancer Cell Proliferation with Partial Involvement of IGF-Associated AKT/mTOR Signaling: A Pilot Translational Study with Exploratory Molecular Insights.International journal of molecular sciences · 2026Article
- From neural loss to regeneration: modulating cell death to enhance pluripotent stem cell graft survival and integration.Cell death & disease · 2026Review
- Restoration of spermatogenesis is dependent on activation of a SPRY4-ERK checkpoint following germline stem cell damage†.Biology of reproduction · 2026Article
- Integrated Transcriptomic and Proteomic Analysis Unveils the Multi-Organ Regulatory Mechanisms of Growth Divergence in Grass Carp (Animals : an open access journal from MDPI · 2026Article
- Dissecting the oncogenic function of YAP1 and WWTR1 fusion proteins in mammary epithelial cells.Cancer letters · 2026Article
954 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
3 authors.
Funding
Abstract
The Ras-extracellular signal-regulated kinase (Ras-ERK) and phosphatidylinositol 3-kinase-mammalian target of rapamycin (PI3K-mTOR) signaling pathways are the chief mechanisms for controlling cell survival, differentiation, proliferation, metabolism, and motility in response to extracellular cues. Components of these pathways were among the first to be discovered when scientists began cloning proto-oncogenes and purifying cellular kinase activities in the 1980s. Ras-ERK and PI3K-mTOR were originally modeled as linear signaling conduits activated by different stimuli, yet even early experiments hinted that they might intersect to regulate each other and co-regulate downstream functions. The extent of this cross-talk and its significance in cancer therapeutics are now becoming clear.
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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.