ArticleThe EMBO journal2010
β-arrestin Kurtz inhibits MAPK and Toll signalling in Drosophila development.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- ERK inhibits Capicua repressor function via multisite phosphorylation.Journal of cell science · 2026Article
- The development of murine bone marrow-derived mast cells expressing functional human MRGPRX2 forFrontiers in immunology · 2024Article
- The Role of Reversible Phosphorylation ofInternational journal of molecular sciences · 2022Review
- The incidence of candidate binding sites for β-arrestin in Drosophila neuropeptide GPCRs.PloS one · 2022Article
- Article
- Normal Ethanol Sensitivity and Rapid Tolerance Require the G Protein Receptor Kinase 2 in Ellipsoid Body Neurons in Drosophila.Alcoholism, clinical and experimental research · 2020Article
- Activation-induced substrate engagement in ERK signaling.Molecular biology of the cell · 2020Article
- Structure-function analysis of β-arrestin Kurtz reveals a critical role of receptor interactions in downregulation of GPCR signaling in vivo.Developmental biology · 2019Article
- Arrestin mutations: Some cause diseases, others promise cure.Progress in molecular biology and translational science · 2019Review
- Quantitative Control of GPCR Organization and Signaling by Endocytosis in Epithelial Morphogenesis.Current biology : CB · 2018Article
- β-Arrestins Negatively Regulate the Toll Pathway in Shrimp by Preventing Dorsal Translocation and Inhibiting Dorsal Transcriptional Activity.The Journal of biological chemistry · 2016Article
- The Fog signaling pathway: insights into signaling in morphogenesis.Developmental biology · 2014Review
- Article
- Potential benefits of therapeutic use of β2-adrenergic receptor agonists in neuroprotection and Parkinsonμs disease.Journal of immunology research · 2014Review
- Regulation of Toll signaling and inflammation by β-arrestin and the SUMO protease Ulp1.Genetics · 2013Article
- Gene dosage-dependent negative regulatory role of β-arrestin-2 in polymicrobial infection-induced inflammation.Infection and immunity · 2013Article
- β-Arrestins in the immune system.Progress in molecular biology and translational science · 2013Review
- Distinct and shared roles of β-arrestin-1 and β-arrestin-2 on the regulation of C3a receptor signaling in human mast cells.PloS one · 2011Article
- Role of the Drosophila non-visual ß-arrestin kurtz in hedgehog signalling.PLoS genetics · 2011Article
- Regulation of C3a receptor signaling in human mast cells by G protein coupled receptor kinases.PloS one · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Arrestins have been implicated in the regulation of multiple signalling pathways. However, their role in organism development is not well understood. In this study, we report a new in vivo function of the Drosophila β-arrestin Kurtz (Krz) in the regulation of two distinct developmental signalling modules: MAPK ERK and NF-κB, which transmit signals from the activated receptor tyrosine kinases (RTKs) and the Toll receptor, respectively. Analysis of the expression of effectors and target genes of Toll and the RTK Torso in krz maternal mutants reveals that Krz limits the activity of both pathways in the early embryo. Protein interaction studies suggest a previously uncharacterized mechanism for ERK inhibition: Krz can directly bind and sequester an inactive form of ERK, thus preventing its activation by the upstream kinase, MEK. A simultaneous dysregulation of different signalling systems in krz mutants results in an abnormal patterning of the embryo and severe developmental defects. Our findings uncover a new in vivo function of β-arrestins and present a new mechanism of ERK inhibition by the Drosophila β-arrestin Krz.
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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.