ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Prohibitins and the cytoplasmic domain of CD86 cooperate to mediate CD86 signaling in B lymphocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- CD86, the double agent: Significance of CD86 expression in B-cell malignancies.International journal of cancer · 2025Review
- Inflammasome functional activities in B lymphocytes.Immunologic research · 2024Article
- Myeloid-derived grancalcin instigates obesity-induced insulin resistance and metabolic inflammation in male mice.Nature communications · 2024Article
- Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024Review
- Prohibitin Expression in Antigen-Presenting Cells: Implications for Inciting Trigger in CNS IgG4-Related Disease.Annals of case reports · 2024Article
- Simultaneous selection of nanobodies for accessible epitopes on immune cells in the tumor microenvironment.Nature communications · 2023Article
- Transcriptome alterations in peripheral blood B cells of patients with multiple sclerosis receiving immune reconstitution therapy.Journal of neuroinflammation · 2023Article
- The prohibitin complex regulates macrophage fatty acid composition, plasma membrane packing, and lipid raft-mediated inflammatory signaling.Prostaglandins, leukotrienes, and essential fatty acids · 2023Article
- Galectin-3 and prohibitin 1 are autoantigens in IgG4-related cholangitis without clear-cut protective effects against toxic bile acids.Frontiers in immunology · 2023Article
- Prohibitin-1 Is a Dynamically Regulated Blood Protein With Cardioprotective Effects in Sepsis.Journal of the American Heart Association · 2021Article
- Activation of the Integrated Stress Response and ER Stress Protect from Fluorizoline-Induced Apoptosis in HEK293T and U2OS Cell Lines.International journal of molecular sciences · 2021Article
- Article
- Prohibitin: a prime candidate for a pleiotropic effector that mediates sex differences in obesity, insulin resistance, and metabolic dysregulation.Biology of sex differences · 2019Review
- Prohibitin: A hypothetical target for sex-based new therapeutics for metabolic and immune diseases.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Electromagnetic fields alter the motility of metastatic breast cancer cells.Communications biology · 2019Article
- The prohibitin protein complex promotes mitochondrial stabilization and cell survival in hematologic malignancies.Oncotarget · 2017Article
- Article
- Prohibitin - At the crossroads of obesity-linked diabetes and cancer.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Neuroendocrine regulation of inflammation.Seminars in immunology · 2014Review
- Novel regulation of CD80/CD86-induced phosphatidylinositol 3-kinase signaling by NOTCH1 protein in interleukin-6 and indoleamine 2,3-dioxygenase production by dendritic cells.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
CD86 engagement on a CD40L/IL-4-primed murine B cell activates signaling intermediates that promote NF-κB activation to increase Oct-2 and mature IgG1 mRNA and protein expression, as well as the rate of IgG1 transcription, without affecting class switch recombination. One of the most proximal signaling intermediates identified is phospholipase Cγ2, a protein reported to bind tyrosine residues, which are absent in the cytoplasmic domain of CD86. Using a proteomics-based identification approach, we show that the tyrosine-containing transmembrane adaptor proteins prohibitin (Phb)1 and Phb2 bind to CD86. The basal expression of Phb1/2 and association with CD86 was low in resting B cells, whereas the level of expression and association increased primarily after priming with CD40. The CD86-induced increase in Oct-2 and IgG1 was less when either Phb1/2 expression was reduced by short hairpin RNA or the cytoplasmic domain of CD86 was truncated or mutated at serine/threonine protein kinase C phosphorylation sites, which did not affect Phb1/2 binding to CD86. Using this approach, we also show that Phb1/2 and the CD86 cytoplasmic domain are required for the CD86-induced phosphorylation of IκBα, which we previously reported leads to NF-κB p50/p65 activation, whereas only Phb1/2 was required for the CD86-induced phosphorylation of phospholipase Cγ2 and protein kinase Cα/β(II), which we have previously reported leads to NF-κB (p65) phosphorylation and subsequent nuclear translocation. Taken together, these findings suggest that Phb1/2 and the CD86 cytoplasmic domain cooperate to mediate CD86 signaling in a B cell through differential phosphorylation of distal signaling intermediates required to increase IgG1.
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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.