ArticleThe Journal of cell biology2005
Merlin/NF-2 mediates contact inhibition of growth by suppressing recruitment of Rac to the plasma membrane.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 2 of them syntheses that pooled it.
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.
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
108 citing papers in PubMed, 2 syntheses or guidelines pooled it, 192 citations in OpenAlex.
- Tumor Microenvironment in Sporadic Vestibular Schwannoma: A Systematic, Narrative Review.International journal of molecular sciences · 2023Pooled it
- Contemporary Molecular Biology of Sporadic Vestibular Schwannomas: A Systematic Review and Clinical Implications.The journal of international advanced otology · 2018Pooled it
- Transient proliferation by reversible YAP and mitogen control of the cyclin D1/p27 ratio.Communications biology · 2026Article
- T-cell-targeted immunotherapy in neurofibromatosis type 2-related vestibular schwannoma: current evidence and future direction.Brain communications · 2026Review
- Recent Advancements in Drug Targeting for Ferroptosis as an Antitumor Therapy: Development of Novel therapeutics.Current cancer drug targets · 2026Review
- Preoperative prediction of brain invasion in meningiomas: a comparison of diffusion kurtosis imaging and diffusion tensor imaging.BMC neurology · 2025Article
- Morphological control of merlin-Rac antagonism in proliferation-promoting signaling.Science signaling · 2025Article
- Current molecular understanding of central nervous system schwannomas.Acta neuropathologica communications · 2025Review
- Review
- The molecular biology of NF2/Merlin on tumorigenesis and development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Gene Therapy for Neurofibromatosis Type 2-Related Schwannomatosis: Recent Progress, Challenges, and Future Directions.Oncology and therapy · 2024Review
- The first embryo, the origin of cancer and animal phylogeny. II. The neoplastic process as an evolutionary engine.Journal of biosciences · 2024Article
- Missense variant interaction scanning reveals a critical role of the FERM domain for tumor suppressor protein NF2 conformation and function.Life science alliance · 2023Article
- The clinical, genetic, and immune landscape of meningioma in patients with NF2-schwannomatosis.Neuro-oncology advances · 2023Article
- Article
- Hallmarks of Cancer Expression in Oral Lichen Planus: A Scoping Review of Systematic Reviews and Meta-Analyses.International journal of molecular sciences · 2022Article
- Article
- Gatekeeping role ofScience advances · 2022Article
- mTOR Signaling and Potential Therapeutic Targeting in Meningioma.International journal of molecular sciences · 2022Review
- Targeting Ferroptosis Pathway to Combat Therapy Resistance and Metastasis of Cancer.Frontiers in pharmacology · 2022Review
48 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 at 1 institution in 1 country.
Funding
Abstract
Introduction of activated p21-activated kinase (PAK) is sufficient to release primary endothelial cells from contact inhibition of growth. Confluent cells display deficient activation of PAK and translocation of Rac to the plasma membrane at matrix adhesions. Targeting Rac to the plasma membrane rescues these cells from contact inhibition. PAK's ability to release human umbilical vein endothelial cells from contact inhibition is blocked by an unphosphorylatable form of its target Merlin, suggesting that PAK promotes mitogenesis by phosphorylating, and thus inactivating, Merlin. Merlin mutants, which are presumed to exert a dominant-negative effect, enable recruitment of Rac to matrix adhesions and promote mitogenesis in confluent cells. Small interference RNA-mediated knockdown of Merlin exerts the same effects. Dominant-negative Rac blocks PAK-mediated release from contact inhibition, implying that PAK functions upstream of Rac in this signaling pathway. These results provide a framework for understanding the tumor suppressor function of Merlin and indicate that Merlin mediates contact inhibition of growth by suppressing recruitment of Rac to matrix adhesions.
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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.