ArticleLeukemia2013
Transcriptional suppression of BACH2 by the Bcr-Abl oncoprotein is mediated by PAX5.
Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Rheumatoid factor production is genetically and molecularly distinct from rheumatoid arthritis.The Journal of clinical investigation · 2026Article
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- Disruption to the FOXO-PRDM1 axis resulting from deletions of chromosome 6 in acute lymphoblastic leukaemia.Leukemia · 2023Article
- IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?International journal of molecular sciences · 2023Review
- Bach2: A Key Regulator in Th2-Related Immune Cells and Th2 Immune Response.Journal of immunology research · 2022Review
- BACH2-mediated FOS confers cytarabine resistance via stromal microenvironment alterations in pediatric ALL.Cancer science · 2021Observational
- Transcriptional Regulation of Genes by Ikaros Tumor Suppressor in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2020Review
- IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression.Nature communications · 2017Article
- Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia.Blood · 2017Article
- BACH transcription factors in innate and adaptive immunity.Nature reviews. Immunology · 2017Review
- The NF-κB subunit c-Rel regulates Bach2 tumour suppressor expression in B-cell lymphoma.Oncogene · 2016Article
- The Bach Family of Transcription Factors: A Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- WT1-mediated repression of the proapoptotic transcription factor ZNF224 is triggered by the BCR-ABL oncogene.Oncotarget · 2015Article
- Transcription factor networks in B-cell differentiation link development to acute lymphoid leukemia.Blood · 2015Review
- Genetic events other than BCR-ABL1.Current hematologic malignancy reports · 2014Review
- BACH2-BCL6 balance regulates selection at the pre-B cell receptor checkpoint.Trends in immunology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bach2 is a lymphoid-specific transcription factor with a prominent role in B-cell development and apoptosis-induction in response to oxidative stress. We previously showed that Bach2 is downregulated in chronic myeloid leukaemia (CML), and here we demonstrate the mechanism by which Bcr-Abl mediates this phenomenon. We have cloned a 3.9 Kb genomic DNA fragment upstream of the transcription initiation site, and delineated the core and proximal BACH2 promoter regions. Transient BCR-ABL expression led to significant reduction in BACH2 promoter activity and this effect was dependent on the kinase function of the oncoprotein. Sequential deletions disclosed several regulatory elements within the promoter region, as well as within BACH2 exonic sequences. Analysis of these elements and transient transfection assays led to the identification of the Pax5 transcription factor as a potent trans-activator of BACH2, whose effect is predominantly mediated through occupation of a binding site on the BACH2 promoter, as demonstrated by both in vitro and in vivo experiments. Overall, our data show that Pax5 functions as an intermediate effector in the Bcr-Abl-mediated transcriptional repression of BACH2. The current results, combined with previous reports, establish Pax5 and Bach2 as transcriptional targets of Bcr-Abl, whose downregulation may contribute to lymphoid blast crisis of CML.
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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.