ArticleNature communications2023
Inherited ARPC5 mutations cause an actinopathy impairing cell motility and disrupting cytokine signaling.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Distinct Arp2/3 isocomplexes drive axonal actin ring assembly and integrity.Science advances · 2026Article
- The actomyosin cortex controls t-tubule remodeling in skeletal muscle.Science advances · 2026Article
- Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The Arp2/3 complex controls the development of homeostatic microglia.EMBO reports · 2026Article
- The Effect of Low Socioeconomic Status on the Leptin-to-Adiponectin Ratio.Nursing open · 2026Review
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- Branched actin networks mediate macrophage-dependent host-microbiota homeostasis.Science (New York, N.Y.) · 2025Article
- A microexon in Arp2 alters tissue-specific Arp2/3-generated actin structures.bioRxiv : the preprint server for biology · 2025Article
- Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by γ-actin.Nature communications · 2025Article
- Proteomic landscape of porcine induced neural stem cell reprogramming and differentiation.PeerJ · 2025Article
- CK-666 and CK-869 differentially inhibit Arp2/3 iso-complexes.EMBO reports · 2024Article
- Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1B.Journal of cell science · 2024Article
Corrections and comments
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Authors and funding
28 authors at 9 institutions in 5 countries.
Funding
Abstract
We describe the first cases of germline biallelic null mutations in ARPC5, part of the Arp2/3 actin nucleator complex, in two unrelated patients presenting with recurrent and severe infections, early-onset autoimmunity, inflammation, and dysmorphisms. This defect compromises multiple cell lineages and functions, and when protein expression is reestablished in-vitro, the Arp2/3 complex conformation and functions are rescued. As part of the pathophysiological evaluation, we also show that interleukin (IL)-6 signaling is distinctively impacted in this syndrome. Disruption of IL-6 classical but not trans-signaling highlights their differential roles in the disease and offers perspectives for therapeutic molecular targets.
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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.