ArticleProceedings of the National Academy of Sciences of the United States of America2007
beta-arrestin 2 oligomerization controls the Mdm2-dependent inhibition of p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Membrane lipid poly-unsaturation selectively affects dopamine D2 receptor endocytosis.Nature communications · 2026Article
- Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies.Genes & diseases · 2025Review
- The PKCι-β-arrestin2 axis disrupts SORLA retrograde trafficking, driving its degradation and amyloid pathology in Alzheimer's disease.Molecular neurodegeneration · 2025Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases.Experimental & molecular medicine · 2024Review
- GPCR targeting of E3 ubiquitin ligase MDM2 by inactive β-arrestin.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A single phenylalanine residue in β-arrestin2 critically regulates its binding to G protein-coupled receptors.The Journal of biological chemistry · 2022Article
- β-arrestin1 promotes tauopathy by transducing GPCR signaling, disrupting microtubules and autophagy.Life science alliance · 2022Article
- Article
- The RanBP2/RanGAP1-SUMO complex gates β-arrestin2 nuclear entry to regulate the Mdm2-p53 signaling axis.Oncogene · 2021Article
- YAP and endothelin-1 signaling: an emerging alliance in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Exploring GPCR-arrestin interfaces with genetically encoded crosslinkers.EMBO reports · 2020Article
- Phosphorylated peptide of G protein-coupled receptor induces dimerization in activated arrestin.Scientific reports · 2020Article
- β-Arrestin2 arrests the clearance of tau in FTLD.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Mdm2 enhances ligase activity of parkin and facilitates mitophagy.Scientific reports · 2020Article
- β-Arrestin2 oligomers impair the clearance of pathological tau and increase tau aggregates.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease.International journal of medical sciences · 2019Article
- S-Nitrosylation of β-Arrestins Biases Receptor Signaling and Confers Ligand Independence.Molecular cell · 2018Article
- Ligand-specific conformational transitions and intracellular transport are required for atypical chemokine receptor 3-mediated chemokine scavenging.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
beta-arrestins (beta-arrs), two ubiquitous proteins involved in serpentine heptahelical receptor regulation and signaling, form constitutive homo- and heterooligomers stabilized by inositol 1,2,3,4,5,6-hexakisphosphate (IP6). Monomeric beta-arrs are believed to interact with receptors after agonist activation, and therefore, beta-arr oligomers have been proposed to represent a resting biologically inactive state. In contrast to this, we report here that the interaction with and subsequent titration out of the nucleus of the protooncogene Mdm2 specifically require beta-arr2 oligomers together with the previously characterized nucleocytoplasmic shuttling of beta-arr2. Mutation of the IP6-binding sites impair oligomerization, reduce interaction with Mdm2, and inhibit p53-dependent antiproliferative effects of beta-arr2, whereas the competence for receptor regulation and signaling is maintained. These observations suggest that the intracellular concentration of beta-arr2 oligomers might control cell survival and proliferation.
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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.