ArticleThe Journal of biological chemistry2012
Annexin A2 and A5 serve as new ligands for C1q on apoptotic cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 111 citations in OpenAlex.
- The role of Annexin A2 in Alzheimer's disease: From cellular functions to therapeutic potential.The FEBS journal · 2026Review
- Rather a versatile multi-tool than a sword: an integral role of the plasminogen system in health and disease.Frontiers in immunology · 2026Review
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Nonapoptotic caspase-3 guides C1q-dependent synaptic phagocytosis by microglia.Nature communications · 2025Article
- Review
- Complement activation drives the phagocytosis of necrotic cell debris and resolution of liver injury.Frontiers in immunology · 2024Article
- Efferocytosis and Respiratory Disease.International journal of molecular sciences · 2023Review
- ANXA2 is a potential biomarker for cancer prognosis and immune infiltration: A systematic pan-cancer analysis.Frontiers in genetics · 2023Article
- C1q and the classical complement cascade in geographic atrophy secondary to age-related macular degeneration.International journal of retina and vitreous · 2022Review
- A Temporal Comparative RNA Transcriptome Profile of the Annexin Gene Family in the Salivary versus Lacrimal Glands of the Sjögren's Syndrome-Susceptible C57BL/6.NOD-International journal of molecular sciences · 2022Article
- Molecular analysis of Annexin expression in cancer.BMC cancer · 2022Article
- Enrichment of Complement, Immunoglobulins, and Autoantibody Targets in the Proteome of Platelets from Patients with Systemic Lupus Erythematosus.Thrombosis and haemostasis · 2022Article
- Synaptic pruning of murine adult-born neurons by microglia depends on phosphatidylserine.The Journal of experimental medicine · 2022Article
- Morphological and Transcriptional Changes in Human Bone Marrow During Natural Plasmodium vivax Malaria Infections.The Journal of infectious diseases · 2022Article
- Microglial heterogeneity and complement component 3 elimination within emerging multisensory midbrain compartments during an early critical period.Frontiers in neuroscience · 2022Article
- Annexin A2 in Fibrinolysis, Inflammation and Fibrosis.International journal of molecular sciences · 2021Review
- Borrelia burgdorferi infection modifies protein content in saliva of Ixodes scapularis nymphs.BMC genomics · 2021Article
- Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Neutrophil Extracellular Traps in Systemic Lupus Erythematosus Stimulate IgG2 Production From B Lymphocytes.Frontiers in medicine · 2021Article
- Advances in cancer treatment: a new therapeutic target, Annexin A2.Journal of Cancer · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q is the initiator of the classical complement pathway and opsonizes apoptotic cells to facilitate phagocytosis. Deficiency of C1q is the strongest known risk factor for development of systemic lupus erythematosus (SLE), which appears to be related to ensuing impaired clearance of apoptotic material. The objective of the current study was to investigate new ligands for C1q on the surface of apoptotic cells. We revealed that the two phospholipid-binding proteins annexin A2 and A5 are, beside DNA, significant C1q ligands. We furthermore, demonstrated that C1q binds directly to histones exposed on the surface of dying cells but we did not detect significant interaction with phosphatidylserine. The complement inhibitors C4b-binding protein and factor H also interact with dying cells, most likely to decrease complement activation beyond the level of C3 to allow noninflammatory clearance. Despite the fact that C4b-binding protein, factor H, and C1q share some ligands on dying cells, we showed that these three proteins did not compete with one another for binding to apoptotic cells. We additionally demonstrated that the way in which apoptosis is induced influenced both the degree of apoptosis and the binding of C1q. The knowledge, that annexin A2 and A5 act as ligands for C1q on apoptotic cells, sheds new light on the pathophysiology of autoimmune diseases.
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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.