ArticleOncogene2011
PAX5-PML acts as a dual dominant-negative form of both PAX5 and PML.
Article in Oncogene, 2011. 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, 42 citations in OpenAlex.
- Two-way inhibition of PAX5 transcriptional activity by PAX5::CBFA2T3.FEBS open bio · 2025Article
- Phase-separating fusion proteins drive cancer by upsetting transcription regulation.Genome biology · 2025Article
- Acute Promyelocytic Leukemia, Retinoic Acid, and Arsenic: A Tale of Dualities.Cold Spring Harbor perspectives in medicine · 2024Review
- Epigenomic mapping reveals distinct B cell acute lymphoblastic leukemia chromatin architectures and regulators.Cell genomics · 2023Article
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- EBF1-JAK2 inhibits the PAX5 function through physical interaction with PAX5 and kinase activity.International journal of hematology · 2023Article
- Functional inhibition of MEF2 by C/EBP is a possible mechanism of leukemia development by CEBP-IGH fusion gene.Cancer science · 2023Article
- The Pleiotropy ofInternational journal of molecular sciences · 2022Review
- The TRIM proteins in cancer: from expression to emerging regulatory mechanisms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Review
- Functional analysis of a novel fusion protein PAX5-KIDINS220 identified in a pediatric Ph-like ALL patient.International journal of hematology · 2020Article
- PML nuclear body biogenesis and oligomerization-driven leukemogenesis.Blood science (Baltimore, Md.) · 2020Review
- B1 oligomerization regulates PML nuclear body biogenesis and leukemogenesis.Nature communications · 2019Article
- PAX5-ELN oncoprotein promotes multistep B-cell acute lymphoblastic leukemia in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- TRIM proteins in blood cancers.Journal of cell communication and signaling · 2018Review
- Differentiation therapy revisited.Nature reviews. Cancer · 2018Review
- Intragenic amplification ofBlood advances · 2017Article
- Molecular role of the PAX5-ETV6 oncoprotein in promoting B-cell acute lymphoblastic leukemia.The EMBO journal · 2017Article
- Induction of Epstein-Barr Virus Oncoprotein LMP1 by Transcription Factors AP-2 and Early B Cell Factor.Journal of virology · 2016Article
- B Cell Linker Protein (BLNK) Is a Selective Target of Repression by PAX5-PML Protein in the Differentiation Block That Leads to the Development of Acute Lymphoblastic Leukemia.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PAX5 is a transcription factor required for B-cell development and maintenance. PML is a tumor suppressor and a pro-apoptotic factor. A fusion gene, PAX5-PML, was found in acute lymphoblastic leukemia (ALL) with chromosomal translocation t(9;15)(p13;q24), but no functional analysis has been reported. Here, we demonstrate that PAX5-PML had a dominant-negative effect on both PAX5 and PML. PAX5-PML dominant negatively inhibited PAX5 transcriptional activity in the luciferase reporter assay and suppressed the expression of the PAX5 transcriptional targets in B-lymphoid cell line. Surprisingly, PAX5-PML hardly showed DNA-binding activity in vitro although it retained the DNA-binding domain of PAX5. Additional experiments, including chromatin immunoprecipitation (ChIP) assay, suggested that PAX5-PML bound to the promoter through the association with PAX5 on the promoter. On the other hand, coexpression of PAX5-PML inhibited PML sumoylation, disrupted PML nuclear bodies (NBs), and conferred apoptosis resistance on HeLa cells. Furthermore, treatment with arsenic trioxide (ATO) induced PML sumoylation and reconstitution of PML NBs, and overcame the anti-apoptotic effect of PAX5-PML in HeLa cells. These data suggest the possible involvement of this fusion protein in the leukemogenesis of B-ALL in a dual dominant-negative manner and the possibility that ALL with PAX5-PML can be treated with ATO.
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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.