ArticleProceedings of the National Academy of Sciences of the United States of America2012
Role for B-cell adapter for PI3K (BCAP) as a signaling adapter linking Toll-like receptors (TLRs) to serine/threonine kinases PI3K/Akt.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.
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Who cites it
114 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Variants in BANK1 are associated with lupus nephritis of European ancestry.Genes and immunity · 2021Pooled it
- Phase I/II trial of everolimus in combination with bortezomib and rituximab (RVR) in relapsed/refractory Waldenstrom macroglobulinemia.Leukemia · 2015Trial
- Article
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- Immunometabolic reprogramming in sepsis: mechanisms, clinical endotypes, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Absence of BCAP in myeloid cells abrogates M2 macrophage differentiation and promotes anti-tumor immunity.iScience · 2025Article
- Notch2 signaling instructs viral and bacterial TLR responsiveness in B cells.bioRxiv : the preprint server for biology · 2025Article
- Insights into PI3K/AKT signaling in B cell development and chronic lymphocytic leukemia.FEBS letters · 2025Review
- Combined Impacts of Acute Heat Stress on the Histology, Antioxidant Activity, Immunity, and Intestinal Microbiota of Wild Female Burbot (Antioxidants (Basel, Switzerland) · 2025Article
- BCAP Is an Interferon-Stimulated Gene That Enhances Type I Interferon Activity in Response to Lipopolysaccharide.International journal of molecular sciences · 2025Article
- Pik3ip1/TrIP Regulation of PI3K Restricts CD8 T Cell Anti-Tumor Immunity.bioRxiv : the preprint server for biology · 2025Article
- Type III interferon primes pDCs for TLR7 activation and antagonizes immune suppression mediated by TGF-β and PGE2.Nature communications · 2025Article
- MyD88 determines T cell fate through BCAP-PI3K signaling.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Targeting persistently activated inflammatory microenvironment to promote chronic wound healing.Frontiers in immunology · 2025Review
- Lactate and lactylation in macrophage polarization of sepsis.Frontiers in cellular and infection microbiology · 2025Review
- Imperative role of adaptor proteins in macrophage toll-like receptor signaling pathways.Future science OA · 2024Review
- Progress in Lactate Metabolism and Its Regulation via Small Molecule Drugs.Molecules (Basel, Switzerland) · 2024Review
- B cell adapter for PI 3-kinase (BCAP) coordinates antigen internalization and trafficking through the B cell receptor.Science advances · 2024Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Toll like receptors (TLRs) use Toll-IL-1 receptor (TIR) domain-containing adapters, such as myeloid differentiation primary response gene 88 (MyD88) and TIR domain-containing adapter inducing IFN-β (TRIF), to induce activation of transcription factors, including NF-κB, MAP kinases, and IFN regulatory factors. TLR signaling also leads to activation of PI3K, but the molecular mechanism is not understood. Here we have discovered a unique role for B-cell adapter for PI3K (BCAP) in the TLR-signaling pathway. We find that BCAP has a functional N-terminal TIR homology domain and links TLR signaling to activation of PI3K. In addition, BCAP negatively regulates proinflammatory cytokine secretion upon TLR stimulation. In vivo, the absence of BCAP leads to exaggerated recruitment of inflammatory myeloid cells following infections and enhanced susceptibility to dextran sulfate sodium-induced colitis. Our results demonstrate that BCAP is a unique TIR domain-containing TLR signaling adapter crucial for linking TLRs to PI3K activation and regulating the inflammatory response.
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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.