ArticleThe Journal of clinical investigation2009
C3b deposition on human erythrocytes induces the formation of a membrane skeleton-linked protein complex.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- RBC membrane biomechanics and Plasmodium falciparum invasion: probing beyond ligand-receptor interactions.Trends in parasitology · 2022Review
- Red Blood Cell Homeostasis and Altered Vesicle Formation in Patients With Paroxysmal Nocturnal Hemoglobinuria.Frontiers in physiology · 2019Article
- Polymorphic factor H-binding activity of CspA protects Lyme borreliae from the host complement in feeding ticks to facilitate tick-to-host transmission.PLoS pathogens · 2018Article
- Complement Depletion Improves Human Red Blood Cell Reconstitution in Immunodeficient Mice.Stem cell reports · 2017Article
- HUS and atypical HUS.Blood · 2017Review
- Article
- Diffusion of glycophorin A in human erythrocytes.Biochimica et biophysica acta · 2016Article
- The durably resistant rice cultivar Digu activates defence gene expression before the full maturation of Magnaporthe oryzae appressorium.Molecular plant pathology · 2016Article
- The mechanics of malaria parasite invasion of the human erythrocyte - towards a reassessment of the host cell contribution.Cellular microbiology · 2016Review
- Ligation of Glycophorin A Generates Reactive Oxygen Species Leading to Decreased Red Blood Cell Function.PloS one · 2016Article
- Malaria: a master lock for deadly parasites.Nature · 2015Article
- Article
- Malarial anemia: digestive vacuole of Plasmodium falciparum mediates complement deposition on bystander cells to provoke hemophagocytosis.Medical microbiology and immunology · 2014Article
- Potential immune mechanisms associated with anemia in Plasmodium vivax malaria: a puzzling question.Infection and immunity · 2014Review
- C4d deposits on the surface of RBCs in trauma patients and interferes with their function.Critical care medicine · 2014Article
- Article
- Membrane protein dynamics and functional implications in mammalian cells.Current topics in membranes · 2013Article
- CD151 restricts the α6 integrin diffusion mode.Journal of cell science · 2012Article
- Membrane compartmentalization in Southeast Asian ovalocytosis red blood cells.British journal of haematology · 2011Article
- Analysis of molecular diffusion by first-passage time variance identifies the size of confinement zones.Biophysical journal · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Decay-accelerating factor (DAF, also known as CD55), a glycosylphosphatidylinositol-linked (GPI-linked) plasma membrane protein, protects autologous cells from complement-mediated damage by inhibiting complement component 3 (C3) activation. An important physical property of GPI-anchored complement regulatory proteins such as DAF is their ability to translate laterally in the plasma membrane. Here, we used single-particle tracking and tether-pulling experiments to measure DAF lateral diffusion, lateral confinement, and membrane skeletal associations in human erythrocyte membranes. In native membranes, most DAF molecules exhibited Brownian lateral diffusion. Fluid-phase complement activation caused deposition of C3b, one of the products of C3 cleavage, onto erythrocyte glycophorin A (GPA). We then determined that DAF, C3b, GPA, and band 3 molecules were laterally immobilized in the membranes of complement-treated cells, and GPA was physically associated with the membrane skeleton. Mass spectrometry analysis further showed that band 3, alpha-spectrin, beta-spectrin, and ankyrin were present in a complex with C3b and GPA in complement-treated cells. C3b deposition was also associated with a substantial increase in erythrocyte membrane stiffness and/or viscosity. We therefore suggest that complement activation stimulates the formation of a membrane skeleton-linked DAF-C3b-GPA-band 3 complex on the erythrocyte surface. This complex may promote the removal of senescent erythrocytes from the circulation.
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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.