ArticleThe Journal of biological chemistry2016
The Transcription Factor Bach2 Is Phosphorylated at Multiple Sites in Murine B Cells but a Single Site Prevents Its Nuclear Localization.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Spatiotemporal dynamics of adoptively transferred stem-like CD8bioRxiv : the preprint server for biology · 2026Article
- Targeting EZH2 in autoimmune diseases: unraveling epigenetic regulation and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Positive coactivator PC4 shows dynamic nucleolar distribution required for rDNA transcription and protein synthesis.Cell communication and signaling : CCS · 2025Article
- ROCK1 promotes B cell differentiation and proteostasis under stress through the heme-regulated proteins, BACH2 and HRI.JCI insight · 2025Article
- Heme regulates protein interactions and phosphorylation of BACH2 intrinsically disordered region in humoral response.iScience · 2025Article
- Review
- Accelerated plasma-cell differentiation in Bach2-deficient mouse B cells is caused by altered IRF4 functions.The EMBO journal · 2024Article
- The role of transcription factors in shaping regulatory T cell identity.Nature reviews. Immunology · 2023Review
- Hierarchical transcriptional network governing heterogeneous T cell exhaustion and its implications for immune checkpoint blockade.Frontiers in immunology · 2023Review
- Role of Ezrin in Asthma-Related Airway Inflammation and Remodeling.Mediators of inflammation · 2022Review
- PI3Kδ coordinates transcriptional, chromatin, and metabolic changes to promote effector CD8Cell reports · 2021Article
- Protocol forSTAR protocols · 2021Article
- Conserved Epigenetic Programming and Enhanced Heme Metabolism Drive Memory B Cell Reactivation.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- PIK3IP1 Promotes Extrafollicular Class Switching in T-Dependent Immune Responses.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- BACH2 drives quiescence and maintenance of resting Treg cells to promote homeostasis and cancer immunosuppression.The Journal of experimental medicine · 2020Article
- Attenuation of TCR-induced transcription by Bach2 controls regulatory T cell differentiation and homeostasis.Nature communications · 2020Article
- Combined Casein Kinase II inhibition and epigenetic modulation in acute B-lymphoblastic leukemia.BMC cancer · 2019Article
- Article
- Zinc finger-IRF composite elements bound by Ikaros/IRF4 complexes function as gene repression in plasma cell.Blood advances · 2018Article
- TNature reviews. Immunology · 2018Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Bach2 regulates the immune system at multiple points, including class switch recombination (CSR) in activated B cells and the function of T cells in part by restricting their terminal differentiation. However, the regulation of Bach2 expression and its activity in the immune cells are still unclear. Here, we demonstrated that Bach2 mRNA expression decreased in Pten-deficient primary B cells. Bach2 was phosphorylated in primary B cells, which was increased upon the activation of the B cell receptor by an anti-immunoglobulin M (IgM) antibody or CD40 ligand. Using specific inhibitors of kinases, the phosphorylation of Bach2 in activated B cells was shown to depend on the phosphatidylinositol 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) pathway. The complex of mTOR and Raptor phosphorylated Bach2 in vitro. We identified multiple new phosphorylation sites of Bach2 by mass spectrometry analysis of epitope-tagged Bach2 expressed in the mature B cell line BAL17. Among the sites identified, serine 535 (Ser-535) was critical for the regulation of Bach2 because a single mutation of Ser-535 abolished cytoplasmic accumulation of Bach2, promoting its nuclear accumulation in pre-B cells, whereas Ser-509 played an auxiliary role. Bach2 repressor activity was enhanced by the Ser-535 mutation in B cells. These results suggest that the PI3K-Akt-mTOR pathway inhibits Bach2 by both repressing its expression and inducing its phosphorylation in B cells.
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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.