ArticleCellular & molecular immunology2024
Rack1 regulates B-cell development and function by binding to and stabilizing the transcription factor Pax5.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- B cells in cancer: functions, mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- RACK1 governs a dual metabolic switch in lung adenocarcinoma through c-Src/G6PD and TRIM21/LDHA Axes.Cell death & disease · 2026Article
- Article
- SMYD3 synergises with RACK1 to promote colorectal cancer lung metastasis by recruiting SMAD3.Cell communication and signaling : CCS · 2026Article
- RACK1 in host immune response to infections: molecular mechanisms and therapeutic potentials.Frontiers in immunology · 2026Review
- A CCL5Cell & bioscience · 2025Article
- A Duality of Function: An Integrative Model of RACK1 as a Switch Between Translational and Signaling Hubs.International journal of molecular sciences · 2025Review
- RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
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Authors and funding
16 authors.
Funding
Abstract
The transcription factor Pax5 activates genes essential for B-cell development and function. However, the regulation of Pax5 expression remains elusive. The adaptor Rack1 can interact with multiple transcription factors and modulate their activation and/or stability. However, its role in the transcriptional control of B-cell fates is largely unknown. Here, we show that CD19-driven Rack1 deficiency leads to pro-B accumulation and a simultaneous reduction in B cells at later developmental stages. The generation of bone marrow chimeras indicates a cell-intrinsic role of Rack1 in B-cell homeostasis. Moreover, Rack1 augments BCR and TLR signaling in mature B cells. On the basis of the aberrant expression of Pax5-regulated genes, including CD19, upon Rack1 deficiency, further exploration revealed that Rack1 maintains the protein level of Pax5 through direct interaction and consequently prevents Pax5 ubiquitination. Accordingly, Mb1-driven Rack1 deficiency almost completely blocks B-cell development at the pro-B-cell stage. Ectopic expression of Pax5 in Rack1-deficient pro-B cells partially rescues B-cell development. Thus, Rack1 regulates B-cell development and function through, at least partially, binding to and stabilizing Pax5.
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