ArticleCell communication and signaling : CCS2012
The adapter protein ADAP is required for selected dendritic cell functions.
Article in Cell communication and signaling : CCS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- A novel adaptor protein, ARAP, orchestrates Fcγ receptor signaling in mouse dendritic cells via Rap1 activation and NF-κB-mediated cytokine production.Immunology and cell biology · 2026Article
- Alternative splicing immune signature for detecting HBV-related hepatocellular carcinoma in peripheral blood mononuclear cells.Biochemistry and biophysics reports · 2025Article
- Molecular control of PDPNhi macrophage subset induction by ADAP as a host defense in sepsis.JCI insight · 2025Article
- Immune Cell-Type Specific Ablation of Adapter Protein ADAP Differentially Modulates EAE.Frontiers in immunology · 2019Article
- Integrin Activation Through the Hematopoietic Adapter Molecule ADAP Regulates Dendritic Development of Hippocampal Neurons.Frontiers in molecular neuroscience · 2016Article
- Recessive thrombocytopenia likely due to a homozygous pathogenic variant in the FYB gene: case report.BMC medical genetics · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe cytosolic adaptor protein ADAP (adhesion and degranulation promoting adapter protein) is expressed by T cells, natural killer cells, myeloid cells and platelets. ADAP is involved in T-cell-receptor-mediated inside-out signaling, which leads to integrin activation, adhesion and reorganization of the actin cytoskeleton. However, little is known about the role of ADAP in myeloid cells. In the present study, we analyzed the function of ADAP in bone-marrow-derived dendritic cells (BMDCs) from ADAP-deficient mice.
resultsADAP-deficient BMDCs showed almost normal levels of antigen uptake, adhesion, maturation, migration from the periphery to the draining lymph nodes, antigen-specific T-cell activation, and production of the proinflammatory cytokines IL-6 and TNF-∝. Furthermore, we provide evidence that the activation of signaling pathways after lipopolysaccharide (LPS) stimulation are not affected by the loss of ADAP. In contrast, ADAP-deficient BMDCs showed defects in CD11c-mediated cellular responses, with significantly diminished production of IL-6, TNF-∝ and IL-10. Actin polymerization was enhanced after CD11c integrin stimulation.
conclusionsIn summary, we propose that the adapter molecule ADAP is critical for selected CD11c integrin-mediated functions of dendritic cells.
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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.