ArticleThe Journal of biological chemistry2016
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.
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 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Two-way inhibition of PAX5 transcriptional activity by PAX5::CBFA2T3.FEBS open bio · 2025Article
- 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
- Differential gene expression of immunity and inflammation genes in colorectal cancer using targeted RNA sequencing.Frontiers in oncology · 2023Article
- Prevalence and Disability-Adjusted Life Year Rates of Asthma in China: Findings from the GBD Study 2019 of the G20.International journal of environmental research and public health · 2022Article
- Review
- C/EBPβ induces B-cell acute lymphoblastic leukemia and cooperates with BLNK mutations.Cancer science · 2021Article
- [Structure and function of B-cell linker and its role in the development of B cell-related diseases].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Leukemia multiclass assessment and classification from Microarray and RNA-seq technologies integration at gene expression level.PloS one · 2019Article
- Article
- High Expression of VAV Gene Family Predicts Poor Prognosis of Acute Myeloid Leukemia.Technology in cancer research & treatmentArticle
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PAX5 is a transcription factor that is required for the development and maintenance of B cells. Promyelocytic leukemia (PML) is a tumor suppressor and proapoptotic factor. The fusion gene PAX5-PML has been identified in acute lymphoblastic leukemia with chromosomal translocation t(9;15)(p13;q24). We have reported previously that PAX5-PML dominant-negatively inhibited PAX5 transcriptional activity and impaired PML function by disrupting PML nuclear bodies (NBs). Here we demonstrated the leukemogenicity of PAX5-PML by introducing it into normal mouse pro-B cells. Arrest of differentiation was observed in PAX5-PML-introduced pro-B cells, resulting in the development of acute lymphoblastic leukemia after a long latency in mice. Among the transactivation targets of PAX5, B cell linker protein (BLNK) was repressed selectively in leukemia cells, and enforced BLNK expression abrogated the differentiation block and survival induced by PAX5-PML, indicating the importance of BLNK repression for the formation of preleukemic state. We also showed that PML NBs were intact in leukemia cells and attributed this to the low expression of PAX5-PML, indicating that the disruption of PML NBs was not required for the PAX5-PML-induced onset of leukemia. These results provide novel insights into the molecular mechanisms underlying the onset of leukemia by PAX5 mutations.
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