ArticleThe Journal of biological chemistry2011
The tumor suppressor hamartin enhances Dbl protein transforming activity through interaction with ezrin.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Ezrin defines TSC complex activation at endosomal compartments through EGFR-AKT signaling.eLife · 2025Article
- Review
- Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021Review
- Hypoxia-induced autophagy drives colorectal cancer initiation and progression by activating the PRKC/PKC-EZR (ezrin) pathway.Autophagy · 2020Article
- Ezrin interacts with the tumor suppressor CHL1 and promotes neuronal differentiation of human neuroblastoma.PloS one · 2020Article
- Macropinocytosis activated by oncogenic Dbl enables specific targeted delivery of Tat/pDNA nano-complexes into ovarian cancer cells.International journal of nanomedicine · 2018Article
- RhoGTPase signalling at epithelial tight junctions: Bridging the GAP between polarity and cancer.The international journal of biochemistry & cell biology · 2015Review
- Dbl3 drives Cdc42 signaling at the apical margin to regulate junction position and apical differentiation.The Journal of cell biology · 2014Article
- Interactome analysis reveals ezrin can adopt multiple conformational states.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Rho guanine nucleotide exchange factor (GEF) Dbl binds to the N-terminal region of ezrin, a member of the ERM (ezrin, radixin, moesin) proteins known to function as linkers between the plasma membrane and the actin cytoskeleton. Here we have characterized the interaction between ezrin and Dbl. We show that binding of Dbl with ezrin involves positively charged amino acids within the region of the pleckstrin homology (PH) domain comprised between β1 and β2 sheets. In addition, we show that Dbl forms a complex with the tuberous sclerosis-1 (TSC-1) gene product hamartin and with ezrin. We demonstrate that hamartin and ezrin are both required for activation of Dbl. In fact, the knock-down of ezrin and hamartin, as well as the expression of a mutant hamartin, unable to bind ezrin, inhibit Dbl transforming and exchange activity. These results suggest that Dbl is regulated by hamartin through association with ezrin.
Indexed as
Identifiers
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.