ArticleFrontiers in immunology2021
The Sez6 Family Inhibits Complement by Facilitating Factor I Cleavage of C3b and Accelerating the Decay of C3 Convertases.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.
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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
32 citing papers in PubMed, 36 citations in OpenAlex.
- Complement Inhibition in the Clinic: Are We Doing Enough to Protect Patients From Infection?European journal of immunology · 2026Review
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- New Analogs of the Compstatin Family of Clinical Complement Inhibitors with Low Picomolar Target Affinity.Journal of medicinal chemistry · 2026Article
- A novel diagnostic serum protein signature for pediatric inflammatory bowel disease.Journal of pediatric gastroenterology and nutrition · 2026Observational
- Genetic background shapes SEZ6L2 autoimmunity and reveals coordinated immune responses linked to neurological dysfunction.bioRxiv : the preprint server for biology · 2026Article
- SEZ6L2 Loss Disrupts Motor Coordination, Cognitive Function, and Synaptic Connectivity.bioRxiv : the preprint server for biology · 2026Article
- Sez6l promotes neuropathic pain via Wnt5a/CaFrontiers in genetics · 2026Article
- Sez6L2 autoimmunity induces cerebellar ataxia in mice.Journal of neuroinflammation · 2025Article
- Seizure-Related Homolog Protein 6 (SEZ6): Biology and Therapeutic Target in Neuroendocrine Carcinomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- A Rare Patient of SEZ6L2 Antibody-Associated Cerebellar Ataxia.Cerebellum (London, England) · 2025Article
- Gene Expression Profiling in the Cortex of Fabp4 Knockout Mice.Neuropsychopharmacology reports · 2025Article
- Article
- Integrated analysis of proteomics and metabolomics in infantile epileptic spasms syndrome.Scientific reports · 2025Article
- Autoimmune cerebellar ataxia associated with anti-SEZ6L2 antibody: report of three cases.Journal of neurology · 2025Article
- A novel and rapid method to purify the human complement opsonin C3b from human plasma.Frontiers in immunology · 2025Article
- Identification of Common Genes for Neuropathic Pain and Parkinson's Disease Based on Bioinformatics Analysis and Their Potential Value in the Diagnosis of Neuropathic Pain.Journal of pain research · 2025Article
- Overexpression of SEZ6L2 and Immune Infiltration in Cancer Based on Gene Image Diagnosis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Genetic background of walking ability and its relationship with leg defects, mortality, and performance traits in turkeys (Meleagris gallopavo).Poultry science · 2024Article
- Unlocking New Horizons in Small-Cell Lung Cancer Treatment: The Onset of Antibody-Drug Conjugates.Cancers · 2023Review
- Image features of anti-SEZ6L2 encephalitis, a rare cause of ataxia and parkinsonism.Journal of neurology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The Sez6 family consists of Sez6, Sez6L, and Sez6L2. Its members are expressed throughout the brain and have been shown to influence synapse numbers and dendritic morphology. They are also linked to various neurological and psychiatric disorders. All Sez6 family members contain 2-3 CUB domains and 5 complement control protein (CCP) domains, suggesting that they may be involved in complement regulation. We show that Sez6 family members inhibit C3b/iC3b opsonization by the classical and alternative pathways with varying degrees of efficacy. For the classical pathway, Sez6 is a strong inhibitor, Sez6L2 is a moderate inhibitor, and Sez6L is a weak inhibitor. For the alternative pathway, the complement inhibitory activity of Sez6, Sez6L, and Sez6L2 all equaled or exceeded the activity of the known complement regulator MCP. Using Sez6L2 as the representative family member, we show that it specifically accelerates the dissociation of C3 convertases. Sez6L2 also functions as a cofactor for Factor I to facilitate the cleavage of C3b; however, Sez6L2 has no cofactor activity toward C4b. In summary, the Sez6 family are novel complement regulators that inhibit C3 convertases and promote C3b degradation.
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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 Socratic graph.