ArticleOncogene2004
Effect of merlin phosphorylation on neurofibromatosis 2 (NF2) gene function.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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
60 citing papers in PubMed, 102 citations in OpenAlex.
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.Research square · 2026Article
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.bioRxiv : the preprint server for biology · 2026Article
- Morphological control of merlin-Rac antagonism in proliferation-promoting signaling.Science signaling · 2025Article
- CircPOLA2 sensitizes non-small cell lung cancer cells to ferroptosis and suppresses tumorigenesis via the Merlin-YAP signaling pathway.iScience · 2024Article
- The molecular biology of NF2/Merlin on tumorigenesis and development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024Article
- CD44 Intracellular Domain: A Long Tale of a Short Tail.Cancers · 2023Review
- 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 genetic landscape and possible therapeutics of neurofibromatosis type 2.Cancer cell international · 2023Review
- WNT5a Signaling through ROR2 Activates the Hippo Pathway to Suppress YAP1 Activity and Tumor Growth.Cancer research · 2023Article
- Article
- Gatekeeping role ofScience advances · 2022Article
- JAM-A signals through the Hippo pathway to regulate intestinal epithelial proliferation.iScience · 2022Article
- Merlin and expanded integrate cell signaling that regulates cyst stem cell proliferation in the Drosophila testis niche.Developmental biology · 2021Article
- NEDD4L-mediated Merlin ubiquitination facilitates Hippo pathway activation.EMBO reports · 2020Article
- Neratinib degrades MST4 via autophagy that reduces membrane stiffness and is essential for the inactivation of PI3K, ERK1/2, and YAP/TAZ signaling.Journal of cellular physiology · 2020Article
- Critical roles of phosphoinositides and NF2 in Hippo pathway regulation.Genes & development · 2020Article
- Upstream regulation of the Hippo-Yap pathway in cardiomyocyte regeneration.Seminars in cell & developmental biology · 2020Review
- Control of cellular responses to mechanical cues through YAP/TAZ regulation.The Journal of biological chemistry · 2019Review
- The Hippo pathway integrates PI3K-Akt signals with mechanical and polarity cues to control tissue growth.PLoS biology · 2019Article
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
The neurofibromatosis 2 (NF2) tumor suppressor gene product, merlin, belongs to the ezrin-radixin-moesin (ERM) subgroup of the Protein 4.1 family, which links cell surface glycoproteins to the actin cytoskeleton. Previous studies have suggested that phosphorylation of merlin, similar to other ERM proteins, may regulate its function. To determine whether merlin phosphorylation has functional consequences for merlin suppression of cell growth and motility, we generated doxycycline-regulatable RT4 schwannoma cell lines that inducibly express full-length merlin with mutations at two potential phosphorylation sites (amino-acid residues S518 and T576). Whereas a mutation at S518 that mimics constitutive phosphorylation (S518D) abrogates the ability of merlin to suppress cell growth and motility, the S518A merlin mutant, which mimics nonphosphorylated merlin, functions equivalently to wild-type merlin. Similar mutations involving T576, the analogous phosphorylation site in ERM proteins important for regulating their function, had no effect. In contrast to other functionally inactive missense merlin mutants, the regulated overexpression of S518D merlin resulted in dramatic changes in cell shape and the elaboration of filopodial extensions. These results provide the first direct demonstration that the S518D merlin mutation, which mimics merlin phosphorylation, impairs not only merlin growth and motility suppression but also leads to an acquisition of a novel phenotype previously ascribed to ERM proteins.
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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.