ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Deleted in Breast Cancer 1 Suppresses B Cell Activation through RelB and Is Regulated by IKKα Phosphorylation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Regulation and Mechanism of Deleted in Breast Cancer-1 on Dendritic Cell Function in Systemic Lupus Erythematosus.MedComm · 2026Article
- Multifaceted roles of CCAR family proteins in the DNA damage response and cancer.Experimental & molecular medicine · 2024Review
- CCAR-1 works together with the U2AF large subunit UAF-1 to regulate alternative splicing.RNA biology · 2024Article
- Mechanistic insights into the dual role of CCAR2/DBC1 in cancer.Experimental & molecular medicine · 2023Review
- Mechanisms of Artemisia scoparia's Anti-Inflammatory Activity in Cultured Adipocytes, Macrophages, and Pancreatic β-Cells.Obesity (Silver Spring, Md.) · 2020Article
- USP22 controls iNKT immunity through MED1 suppression of histone H2A monoubiquitination.The Journal of experimental medicine · 2020Article
- Inhibitory-κB Kinase (IKK) α and Nuclear Factor-κB (NFκB)-Inducing Kinase (NIK) as Anti-Cancer Drug Targets.Cells · 2018Review
- Loss of DBC1 (CCAR2) affects TNFα-induced lipolysis andJournal of molecular endocrinology · 2018Article
- The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation.Cell reports · 2017Article
- A novel crosstalk between CCAR2 and AKT pathway in the regulation of cancer cell proliferation.Cell death & disease · 2016Article
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Authors and funding
10 authors.
Funding
Abstract
Alternative NF-κB signaling is crucial for B cell activation and Ig production, and it is mainly regulated by the inhibitor of κ B kinase (IKK) regulatory complex. Dysregulation of alternative NF-κB signaling in B cells could therefore lead to hyperactive B cells and Ig overproduction. In our previous, study we found that deleted in breast cancer 1 (DBC1) is a suppressor of the alternative NF-κB pathway to attenuate B cell activation. In this study, we report that loss of DBC1 results in spontaneous overproduction of Ig in mice after 10 mo of age. Using a double mutant genetic model, we confirm that DBC1 suppresses B cell activation through RelB inhibition. At the molecular level, we show that DBC1 interacts with alternative NF-κB members RelB and p52 through its leucine zipper domain. In addition, phosphorylation of DBC1 at its C terminus by IKKα facilitates its interaction with RelB and IKKα, indicating that DBC1-mediated suppression of alternative NF-κB is regulated by IKKα. Our results define the molecular mechanism of DBC1 inhibition of alternative NF-κB activation in suppressing B cell activation.
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