ArticleDevelopmental cell2013
A network of interactions enables CCM3 and STK24 to coordinate UNC13D-driven vesicle exocytosis in neutrophils.
Article in Developmental cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Rho-associated kinase inhibitors in cerebral cavernous malformations: a preclinical systematic review.Neurosurgical review · 2026Pooled it
- Genome-wide association, single-cell, and spatial transcriptomics analyses reveal the role of the STK24-expressing positive cells in LUAD progression and the tumor microenvironment, identifying STK24 as a potential therapeutic target.Journal of translational medicine · 2025Article
- Programmed Cell Death Protein 10 (PDCD10) Regulates Vesicle Trafficking and Contributes to the Progression of Clear Cell Renal Cell Carcinoma.Journal of extracellular vesicles · 2025Article
- Cerebral Cavernous Malformation: From Genetics to Pharmacotherapy.Brain and behavior · 2025Review
- Evolution of chromosome-arm aberrations in breast cancer through genetic network rewiring.Cell reports · 2024Article
- Protein Kinase STK24 Promotes Tumor Immune Evasion via the AKT-PD-L1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Functional role of UNC13D in immune diseases and its therapeutic applications.Frontiers in immunology · 2024Review
- Molecular mechanisms involved in regulating protein activity and biological function of MST3.Cell division · 2023Review
- Endothelial Cell-Pericyte Interactions in the Pathogenesis of Cerebral Cavernous Malformations (CCMs).Cold Spring Harbor perspectives in medicine · 2023Review
- KRIT1-mediated regulation of neutrophil adhesion and motility.The FEBS journal · 2023Article
- Review
- Severe COVID-19 Shares a Common Neutrophil Activation Signature with Other Acute Inflammatory States.Cells · 2022Article
- CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- The multifacetedGenes & diseases · 2021Review
- Pdcd10-Stk24/25 complex controls kidney water reabsorption by regulating Aqp2 membrane targeting.JCI insight · 2021Article
- A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes' interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19.PLoS computational biology · 2021Article
- Caveolae-mediated Tie2 signaling contributes to CCM pathogenesis in a brain endothelial cell-specific Pdcd10-deficient mouse model.Nature communications · 2021Article
- High Levels of Receptor Tyrosine Kinases in CCM3-Deficient Cells Increase Their Susceptibility to Tyrosine Kinase Inhibition.Biomedicines · 2020Article
- Unc-13 homolog D mediates an antiviral effect of the chromosome 19 microRNA cluster miR-517a.Journal of cell science · 2020Article
- Signalling through cerebral cavernous malformation protein networks.Open biology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Neutrophil degranulation plays an important role in acute innate immune responses and is tightly regulated because the granule contents can cause tissue damage. However, this regulation remains poorly understood. Here, we identify the complex of STK24 and CCM3 as being an important regulator of neutrophil degranulation. Lack of either STK24 or CCM3 increases the release of a specific granule pool without affecting other neutrophil functions. STK24 appears to suppress exocytosis by interacting and competing with UNC13D C2B domain for lipid binding, whereas CCM3 has dual roles in exocytosis regulation. Although CCM3 stabilizes STK24, it counteracts STK24-mediated inhibition of exocytosis by recruiting STK24 away from the C2B domain through its Ca(2+)-sensitive interaction with UNC13D C2A domain. This STK24/CCM3-regulated exocytosis plays an important role in the protection of kidneys from ischemia-reperfusion injury. Together, these findings reveal a function of the STK24 and CCM3 complex in the regulation of ligand-stimulated exocytosis.
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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.