ArticleThe Journal of cell biology2025
STIM1/2 maintain signaling competence at ER-PM contact sites during neutrophil spreading.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Interplay between store-operated calcium entry and mitochondrial phosphate handling modulates force and fatigue during exercise.bioRxiv : the preprint server for biology · 2026Article
- The paracrine factor myeloid derived growth factor regulates the inflammatory fate and motility of human induced pluripotent stem cell-derived neutrophils.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Integrin activation by two independently regulated calcium-mediated pathways is required for neutrophil recruitment.Cell communication and signaling : CCS · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Neutrophils are highly motile leukocytes that migrate inside tissues to destroy invading pathogens. Ca2+ signals coordinate leukocytes migration, but whether Ca2+ fluxes mediated by Stim proteins at ER-PM contact sites regulate neutrophil actin-based motility is unclear. Here, we show that myeloid-specific Stim1/2 ablation decreases basal cytosolic Ca2+ levels and prevents adhesion-induced Ca2+ elevations in mouse neutrophils, reducing actin fiber formation and impairing spreading. Unexpectedly, more ER-PM contact sites were detected on the actin-poor adhesive membranes of Stim1/2-deficient neutrophils, which had reduced inositol-1,4,5-trisphosphate receptor (IP3R) immunoreactivity on confocal and immunogold micrographs despite preserved IP3R levels on western blots. Remarkably, Stim1/2-deficient neutrophils regained signaling and spreading competence in Ca2+-rich solutions and were recruited more effectively in mouse inflamed cremaster muscles in vivo. Our findings indicate that Stim1/2 preserve IP3R functionality in neutrophils, generating adhesion-dependent Ca2+ signals that control actin dynamics during neutrophil spreading. Stim proteins thus maintain IP3R signaling competence at adhesive membranes, enabling Ca2+-dependent actin remodeling during spreading in mouse neutrophils.
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