ArticleNature communications2019
Protein prenylation restrains innate immunity by inhibiting Rac1 effector interactions.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Statins and Myasthenia Gravis: Clinical Implications and Pathogenesis.International journal of molecular sciences · 2026Review
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- Shared Plant-human Biology: Herbicide Effects and New Biomarkers Perspectives.Current environmental health reports · 2026Review
- Epigenetic modifications of immune cells in rheumatoid arthritis.Annals of medicine · 2025Review
- Pyrin inflammasome-driven erosive arthritis caused by unprenylated RHO GTPase signaling.EMBO molecular medicine · 2025Article
- Impact of protein prenylation inhibition onJournal of bacteriology · 2025Article
- IQGAP1 participates in bone marrow-derived macrophage recruitment and involves in liver inflammation/fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Protein prenylation in islet β-cell function in health and metabolic stress.Biochemical pharmacology · 2025Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Myeloid PGGT1B Deficiency Promotes Psoriasiform Dermatitis by Promoting the Secretion of Inflammatory Factors.International journal of molecular sciences · 2025Article
- Geranylgeranyl diphosphate synthase deficiency impairs efferocytosis and resolution of acute lung injury.Respiratory research · 2025Article
- Regulation of glial ApoE secretion by the mevalonate pathway is independent of ApoE isoform.Journal of Alzheimer's disease : JAD · 2025Article
- Farnesyl pyrophosphate potentiates dendritic cell migration in autoimmunity through mitochondrial remodelling.Nature metabolism · 2024Article
- Decreased Tiam1-mediated Rac1 activation is responsible for impaired directional persistence of chondrocyte migration in microtia.Journal of cellular and molecular medicine · 2024Article
- IQGAP1 Regulates Actin Polymerization and Contributes to Bleomycin-Induced Lung Fibrosis.International journal of molecular sciences · 2024Article
- Protein lipidation in health and disease: molecular basis, physiological function and pathological implication.Signal transduction and targeted therapy · 2024Review
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- E3 Ubiquitin LigaseCancers · 2023Article
- Sex-based Dysregulation of Inflammation-related Genes in Periodontitis.International journal of molecular and cellular medicine · 2023Article
- Metabolic signature and proteasome activity controls synovial migration ofFrontiers in immunology · 2023Article
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Authors and funding
14 authors at 5 institutions in 5 countries.
Funding
Abstract
Rho family proteins are prenylated by geranylgeranyltransferase type I (GGTase-I), which normally target proteins to membranes for GTP-loading. However, conditional deletion of GGTase-I in mouse macrophages increases GTP-loading of Rho proteins, leading to enhanced inflammatory responses and severe rheumatoid arthritis. Here we show that heterozygous deletion of the Rho family gene Rac1, but not Rhoa and Cdc42, reverses inflammation and arthritis in GGTase-I-deficient mice. Non-prenylated Rac1 has a high affinity for the adaptor protein Ras GTPase-activating-like protein 1 (Iqgap1), which facilitates both GTP exchange and ubiquitination-mediated degradation of Rac1. Consistently, inactivating Iqgap1 normalizes Rac1 GTP-loading, and reduces inflammation and arthritis in GGTase-I-deficient mice, as well as prevents statins from increasing Rac1 GTP-loading and cytokine production in macrophages. We conclude that blocking prenylation stimulates Rac1 effector interactions and unleashes proinflammatory signaling. Our results thus suggest that prenylation normally restrains innate immune responses by preventing Rac1 effector interactions.
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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.