ArticleCellular & molecular immunology2020
BANK1 interacts with TRAF6 and MyD88 in innate immune signaling in B cells.
Article in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
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- Genome-wide association study of frailty and integrative functional analysis to elucidate its relationship with aging.GeroScience · 2026Article
- Acute Sleep Deprivation and the Autoimmune TLR-BANK1 Pathway: Interplay with Gender and Emotional State.International journal of molecular sciences · 2025Article
- Polyporusterone B Alleviates Inflammatory Injury via Suppression of Pro-Inflammatory Cytokine Production.International journal of molecular sciences · 2025Article
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- Molecular mechanism of IKK catalytic dimer docking to NF-κB substrates.Nature communications · 2024Article
- Disruption of KLHL6 Fuels Oncogenic Antigen Receptor Signaling in B-Cell Lymphoma.Blood cancer discovery · 2024Article
- Bank1 modulates the differentiation and molecular profile of key B cell populations in autoimmunity.JCI insight · 2024Article
- 4-1BB-encoding CAR causes cell death via sequestration of the ubiquitin-modifying enzyme A20.Cellular & molecular immunology · 2024Article
- PTEN acts as a crucial inflammatory checkpoint controlling TLR9/IL-6 axis in B cells.iScience · 2024Article
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- Neuropsychiatric involvement in juvenile-onset systemic lupus erythematosus (jSLE).Molecular and cellular pediatrics · 2023Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence supports a possible role of BANK1 in innate immune signaling in B cells. In the present study, we investigated the interaction of BANK1 with two key mediators in interferon and inflammatory cytokine production, TRAF6 and MyD88. We revealed by coimmunoprecipitation (CoIP) analyses the binding of BANK1 with TRAF6 and MyD88, which were mediated by the BANK1 Toll/interleukin-1 receptor (TIR) domain. In addition, the natural BANK1-40C variant showed increased binding to MyD88. Next, we demonstrated in mouse splenic B cells that BANK1 colocalized with Toll-like receptor (TLR) 7 and TLR9 and that after stimulation with TLR7 and TLR9 agonists, the number of double-positive BANK1-TLR7, -TLR9, -TRAF6, and -MyD88 cells increased. Furthermore, we identified five TRAF6-binding motifs (BMs) in BANK1 and confirmed by point mutations and decoy peptide experiments that the C-terminal domain of BANK1-full-length (-FL) and the N-terminal domain of BANK1-Delta2 (-D2) are necessary for this binding. Functionally, we determined that the absence of the TIR domain in BANK1-D2 is important for its lysine (K)63-linked polyubiquitination and its ability to produce interleukin (IL)-8. Overall, our study describes a specific function of BANK1 in MyD88-TRAF6 innate immune signaling in B cells, clarifies functional differences between the two BANK1 isoforms and explains for the first time a functional link between autoimmune phenotypes including SLE and the naturally occurring BANK1-40C variant.
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