ArticleMolecular and cellular biology2005
Akt-dependent cell size regulation by the adhesion molecule on glia occurs independently of phosphatidylinositol 3-kinase and Rheb signaling.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 34 citations in OpenAlex.
- Metabolic and behavioral effects of neurofibromin result from differential recruitment of MAPK and mTOR signaling.PLoS genetics · 2026Article
- Connecting the Dots: AMOG/βInternational journal of molecular sciences · 2025Review
- In silico studies provide new structural insights into trans-dimerization of β1 and β2 subunits of the Na+, K+-ATPase.PloS one · 2025Article
- The βInternational journal of molecular sciences · 2022Article
- Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021Review
- SPOCK1: a multi-domain proteoglycan at the crossroads of extracellular matrix remodeling and cancer development.American journal of cancer research · 2020Review
- Cell Adhesion Molecules and Protein Synthesis Regulation in Neurons.Frontiers in molecular neuroscience · 2020Review
- Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.BMC cancer · 2019Article
- The Na, K-ATPase β-Subunit Isoforms Expression in Glioblastoma Multiforme: Moonlighting Roles.International journal of molecular sciences · 2017Article
- Protein kinase C and P2Y12 take center stage in thrombin-mediated activation of mammalian target of rapamycin complex 1 in human platelets.Journal of thrombosis and haemostasis : JTH · 2014Article
- Na⁺/K⁺-ATPase β2-subunit (AMOG) expression abrogates invasion of glioblastoma-derived brain tumor-initiating cells.Neuro-oncology · 2013Article
- Neurofibromatosis-1 regulates mTOR-mediated astrocyte growth and glioma formation in a TSC/Rheb-independent manner.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Pi3K-mTOR signaling and AMOG expression in epilepsy-associated glioneuronal tumors.Brain pathology (Zurich, Switzerland) · 2010Article
- Neurotrophic factors and structural plasticity in addiction.Neuropharmacology · 2009Review
- Potentiation of astrogliogenesis by STAT3-mediated activation of bone morphogenetic protein-Smad signaling in neural stem cells.Molecular and cellular biology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The role of cell adhesion molecules in mediating interactions with neighboring cells and the extracellular matrix has long been appreciated. More recently, these molecules have been shown to modulate intracellular signal transduction cascades critical for cell growth and proliferation. Expression of adhesion molecule on glia (AMOG) is downregulated in human and mouse gliomas, suggesting that AMOG may be important for growth regulation in the brain. In this report, we examined the role of AMOG expression on cell growth and intracellular signal transduction. We show that AMOG does not negatively regulate cell growth in vitro or in vivo. Instead, expression of AMOG in AMOG-deficient cells results in a dramatic increase in cell size associated with protein kinase B/Akt hyperactivation, which occurs independent of phosphatidylinositol 3-kinase activation. AMOG-mediated Akt phosphorylation specifically activates the mTOR/p70S6 kinase pathway previously implicated in cell size regulation, but it does not depend on tuberous sclerosis complex/Ras homolog enriched in brain (Rheb) signaling. These data support a novel role for a glial adhesion molecule in cell size regulation through selective activation of the Akt/mTOR/S6K signal transduction pathway.
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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.