ArticleScience advances2023
Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Immune dysregulation in the prostates of C57BL/6The Journal of pathology · 2026Article
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Apoptotic vesicles: from biological characteristics to clinical translational prospects.Journal of translational medicine · 2026Review
- Optineurin restrains CCR7 degradation to guide type II collagen-stimulated dendritic cell migration in rheumatoid arthritis.Acta pharmaceutica Sinica. B · 2025Article
- Development of machine learning models for diagnostic biomarker identification and immune cell infiltration analysis in PCOS.Journal of ovarian research · 2025Article
- Enhancing radiotherapy response via intratumoral injection of a TLR9 agonist in autochthonous murine sarcomas.JCI insight · 2024Article
- Single-Nuclei Characterization of Lacrimal Gland in Scopolamine-Induced Dry Eye Disease.Investigative ophthalmology & visual science · 2024Article
- Enhancing radiotherapy response via intratumoral injection of the TLR9 agonist CpG to stimulate CD8 T cells in an autochthonous mouse model of sarcoma.bioRxiv : the preprint server for biology · 2024Article
- Intron retention as an excellent marker for diagnosing depression and for discovering new potential pathways for drug intervention.Frontiers in psychiatry · 2024Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migratory dendritic cells (migDCs) continuously patrol tissues and are activated by injury and inflammation. Extracellular adenosine triphosphate (ATP) is released by damaged cells or actively secreted during inflammation and increases migDC motility. However, the underlying molecular mechanisms by which ATP accelerates migDC migration is not understood. Here, we show that migDCs can be distinguished from other DC subsets and immune cells by their expression of the voltage-gated calcium channel subunit β3 (Cavβ3; CACNB3), which exclusively facilitates ATP-dependent migration in vitro and during tissue damage in vivo. By contrast, CACNB3 does not regulate lipopolysaccharide-dependent migration. Mechanistically, CACNB3 regulates ATP-dependent inositol 1,4,5-trisphophate receptor-controlled calcium release from the endoplasmic reticulum. This, in turn, is required for ATP-mediated suppression of adhesion molecules, their detachment, and initiation of migDC migration. Thus,
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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.