ArticleThe Journal of biological chemistry2008
Endothelial cell annexin A2 regulates polyubiquitination and degradation of its binding partner S100A10/p11.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 130 citations in OpenAlex.
- Inhibition of Langerhans cell maturation by human papillomavirus type 16: a novel role for the annexin A2 heterotetramer in immune suppression.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- ANXA2 as a Candidate Molecular Hub Linking Fibrinolysis, Coagulation, and Immune Remodeling in Hepatocellular Carcinoma: An Integrative Multi-Omics Analysis.International journal of molecular sciences · 2026Article
- Systematic identification of p11 as a signaling modulator across the GPCRome.Science advances · 2026Article
- The role of Annexin A2 in Alzheimer's disease: From cellular functions to therapeutic potential.The FEBS journal · 2026Review
- The Calcium-Binding Protein S100A10 (p11) Is Required for Normal Motor Performance by Regulating Vesicle Dynamics at Excitatory Synapses.Acta physiologica (Oxford, England) · 2026Article
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- A proximity proteomics pipeline with improved reproducibility and throughput.Molecular systems biology · 2024Article
- Annexin A2: A Double-Edged Sword in Pathogen Infection.Pathogens (Basel, Switzerland) · 2024Review
- Opportunistic pathogeniScience · 2024Article
- Cancer-associated thrombosis in hematologic malignancies.International journal of hematology · 2024Review
- A proximity proteomics pipeline with improved reproducibility and throughput.bioRxiv : the preprint server for biology · 2024Article
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- Article
- Translational implications of targeting annexin A2: From membrane repair to muscular dystrophy, cardiovascular disease and cancer.Clinical and translational discovery · 2023Article
- Recent Advances in Molecular and Cellular Functions of S100A10.Biomolecules · 2023Review
- Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours by inhibiting ANXA2 degradation.Cellular and molecular life sciences : CMLS · 2023Article
- Aspergillus fumigatus hijacks human p11 to redirect fungal-containing phagosomes to non-degradative pathway.Cell host & microbe · 2023Article
- Collagen-I influences the post-translational regulation, binding partners and role of Annexin A2 in breast cancer progression.Frontiers in oncology · 2023Article
- InJournal of clinical medicine · 2022Article
- Extracellular Vesicles and Thrombogenicity in Atrial Fibrillation.International journal of molecular sciences · 2022Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The annexin A2 (A2) heterotetramer, consisting of two copies of A2 and two copies of S100A10/p11, promotes fibrinolytic activity on the surface of vascular endothelial cells by assembling plasminogen and tissue plasminogen activator (tPA) and accelerating the generation of plasmin. In humans, overexpression of A2 by acute promyelocytic leukemia cells is associated with excessive fibrinolysis and hemorrhage, whereas anti-A2 autoantibodies appear to accentuate the risk of thrombosis in patients with anti-phospholipid syndrome. Complete deficiency of A2 in mice leads to a lack of tPA cofactor activity, accumulation of intravascular fibrin, and failure to clear arterial thrombi. Within the endothelial cell, p11 is required for Src kinase-mediated tyrosine phosphorylation of A2, which signals translocation of both proteins to the cell surface. Here we show that p11 is expressed at very low levels in the absence of A2 both in vitro and in vivo. We demonstrate further that unpartnered p11 becomes polyubiquitinated and degraded via a proteasome-dependent mechanism. A2 stabilizes intracellular p11 through direct binding, thus masking an autonomous p11 polyubiquitination signal that triggers proteasomal degradation. This interaction requires both the p11-binding N-terminal domain of A2 and the C-terminal domain of p11. This mechanism prevents accumulation of free p11 in the endothelial cell and suggests that regulation of tPA-dependent cell surface fibrinolytic activity is precisely tuned to the intracellular level of p11.
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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.