ArticleThe Journal of biological chemistry2011
Identification of transcription factor E3 (TFE3) as a receptor-independent activator of Gα16: gene regulation by nuclear Gα subunit and its activator.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Identification of a small molecule that targets activator of G-protein signaling 8.The journal of physiological sciences : JPS · 2026Article
- Mechanisms of Location Bias in G Protein-Coupled Receptors.Handbook of experimental pharmacology · 2026Review
- Review
- MAZ51 Blocks the Tumor Growth of Prostate Cancer by Inhibiting Vascular Endothelial Growth Factor Receptor 3.Frontiers in pharmacology · 2021Article
- Review
- Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells.The journal of physiological sciences : JPS · 2020Article
- Activator of G-protein signaling 8 is involved in VEGF-induced choroidal neovascularization.Scientific reports · 2019Article
- The Tnfaip8-PE complex is a novel upstream effector in the anti-autophagic action of insulin.Scientific reports · 2017Article
- Article
- Direct Coupling of a Seven-Transmembrane-Span Receptor to a Gαi G-Protein Regulatory Motif Complex.Molecular pharmacology · 2015Article
- Heterotrimeric G protein-mediated signaling and its non-canonical regulation in the heart.Life sciences · 2015Review
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
- Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.Journal of molecular histology · 2015Article
- Accessory proteins for heterotrimeric G-proteins in the kidney.Frontiers in physiology · 2015Review
- Activators of G protein signaling exhibit broad functionality and define a distinct core signaling triad.Molecular pharmacology · 2014Review
- Protection of cardiomyocytes from the hypoxia-mediated injury by a peptide targeting the activator of G-protein signaling 8.PloS one · 2014Article
- Translocation of activator of G-protein signaling 3 to the Golgi apparatus in response to receptor activation and its effect on the trans-Golgi network.The Journal of biological chemistry · 2013Article
- G protein-coupled receptor signalling in the cardiac nuclear membrane: evidence and possible roles in physiological and pathophysiological function.The Journal of physiology · 2012Review
- Non-canonical signaling and localizations of heterotrimeric G proteins.Cellular signalling · 2012Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Receptor-independent G-protein regulators provide diverse mechanisms for signal input to G-protein-based signaling systems, revealing unexpected functional roles for G-proteins. As part of a broader effort to identify disease-specific regulators for heterotrimeric G-proteins, we screened for such proteins in cardiac hypertrophy using a yeast-based functional screen of mammalian cDNAs as a discovery platform. We report the identification of three transcription factors belonging to the same family, transcription factor E3 (TFE3), microphthalmia-associated transcription factor, and transcription factor EB, as novel receptor-independent activators of G-protein signaling selective for Gα(16). TFE3 and Gα(16) were both up-regulated in cardiac hypertrophy initiated by transverse aortic constriction. In protein interaction studies in vitro, TFE3 formed a complex with Gα(16) but not with Gα(i3) or Gα(s). Although increased expression of TFE3 in heterologous systems had no influence on receptor-mediated Gα(16) signaling at the plasma membrane, TFE3 actually translocated Gα(16) to the nucleus, leading to the induction of claudin 14 expression, a key component of membrane structure in cardiomyocytes. The induction of claudin 14 was dependent on both the accumulation and activation of Gα(16) by TFE3 in the nucleus. These findings indicate that TFE3 and Gα(16) are up-regulated under pathologic conditions and are involved in a novel mechanism of transcriptional regulation via the relocalization and activation of Gα(16).
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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.