ArticleProtein & cell2010
The class A macrophage scavenger receptor type I (SR-AI) recognizes complement iC3b and mediates NF-κB activation.
Article in Protein & cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 37 citations in OpenAlex.
- Enhancing AAV-microdystrophin gene therapy after repeat dosing by blocking phagocytosis.Frontiers in immunology · 2025Article
- Targeting macrophage M1 polarization suppression through PCAF inhibition alleviates autoimmune arthritis via synergistic NF-κB and H3K9Ac blockade.Journal of nanobiotechnology · 2023Article
- Inflammation balance in skeletal muscle damage and repair.Frontiers in immunology · 2023Review
- Article
- Quantitative proteome analysis of temporally resolved phagosomes following uptake via key phagocytic receptors.Molecular & cellular proteomics : MCP · 2015Article
- Differential gene expression in laboratory strains of human head and body lice when challenged with Bartonella quintana, a pathogenic bacterium.Insect molecular biology · 2014Article
- The role of macrophage class a scavenger receptors in a laser-induced murine choroidal neovascularization model.Investigative ophthalmology & visual science · 2013Article
- The evolution of the class A scavenger receptors.BMC evolutionary biology · 2012Article
- The meningococcal adhesin NhhA provokes proinflammatory responses in macrophages via toll-like receptor 4-dependent and -independent pathways.Infection and immunity · 2012Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The macrophage scavenger receptor SR-AI binds to host tissue debris to perform clearance and it binds to bacteria for phagocytosis. In addition, SR-AI modulates macrophage activation through cell signaling. However, investigation of SR-AI signaling on macrophages is complicated due to its promiscuous ligand specificity that overlaps with other macrophage receptors. Therefore, we expressed SR-AI on HEK 293T cells to investigate its ligand binding and signaling. On 293Tcells, SR-AI could respond to E. coli DH5α, leading to NF-κB activation and IL-8 production. However, this requires E. coli DH5α to be sensitized by fresh serum that is treated with heat-inactivation or complement C3 depletion. Anti-C3 antibody inhibits the binding of SR-AI to serum-sensitized DH5α and blocks DH5α stimulation of SR-AI signaling. Further analysis showed that SR-AI can directly bind to purified iC3b but not C3 or C3b. By mutagenesis, The SRCR domain of SR-AI was found to be essential in SR-AI binding to serum-sensitized DH5α. These results revealed a novel property of SR-AI as a complement receptor for iC3b-opsonized bacteria that can elicit cell signaling.
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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.