Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Defective Neutrophil Transendothelial Migration and Lateral Motility in ARPC1B Deficiency Under Flow Conditions.

Frontiers in immunology - 1 Jan 2021

Kempers Lanette, Sprenkeler Evelien G G, van Steen Abraham C I, van Buul Jaap D, Kuijpers Taco W

Abstract excerpt

The actin-related protein (ARP) 2/3 complex, essential for organizing and nucleating branched actin filaments, is required for several cellular immune processes, including cell migration and granule exocytosis. Recently, genetic defects in ARPC1B, a subunit of this complex, were reported. Mutations in ARPC1B result in defective ARP2/3-dependent actin filament branching, leading to a combined immunodeficiency with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Actin-Related Protein 2-3 Complex
Share to Cell Adhesion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chemotaxis

Share to Human Umbilical Vein Endothelial Cells

Share to Neutrophil Infiltration

Share to Neutrophils

Share to Polymerization

Share to Primary Immunodeficiency Diseases

Source

Open in PubMed Open full text

Identifiers

PMID: 34135903
DOI: 10.3389/fimmu.2021.678030
PMCID: PMC8202084

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Defective Neutrophil Transendothelial Migration and Lateral Motility in ARPC1B Deficiency Under Flow Conditions.PMID 34135903Read ↗

Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1BSemantic proximity Read ↗

Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1BSemantic proximity Read ↗

Arp2/3 Complex Is Required for Macrophage Integrin Functions but Is Dispensable for FcR Phagocytosis and In Vivo Motility.Semantic proximity Read ↗

Loss of the Arp2/3 complex component ARPC1B causes platelet abnormalities and predisposes to inflammatory disease.Semantic proximity Read ↗

Arp2/3 complex-dependent actin regulation protects the survival of tissue-resident mast cellsSemantic proximity Read ↗

Emerging functions of cytoskeletal proteins in immune diseasesSemantic proximity Read ↗

Actin dynamics regulation by TTC7A/PI4KIIIα axis limits DNA damage and cell death during leukocyte migrationSemantic proximity Read ↗

Loss of Arp2/3 induces an NF-κB–dependent, nonautonomous effect on chemotactic signalingSemantic proximity Read ↗

Actin dynamics regulation by TTC7A/PI4KIIIα limits DNA damage and cell death under confinement.Semantic proximity Read ↗

Whole-genome screens reveal regulators of differentiation state and context-dependent migration in human neutrophilsSemantic proximity Read ↗

Whole blood human neutrophil trafficking in a microfluidic model of infection and inflammationSemantic proximity Read ↗

Technical Advance: Changes in neutrophil migration patterns upon contact with platelets in a microfluidic assay.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.