ArticleOncogene2005
Evi3, a zinc-finger protein related to EBFAZ, regulates EBF activity in B-cell leukemia.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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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
19 citing papers in PubMed, 33 citations in OpenAlex.
- ZNF521 promotes acute myeloid leukemogenesis by suppressing the expression and acetylation of SMC3.Heliyon · 2024Article
- The ClassicGenetics · 2020Article
- Zinc Finger Protein 521 Regulates Early Hematopoiesis through Cell-Extrinsic Mechanisms in the Bone Marrow Microenvironment.Molecular and cellular biology · 2018Article
- Interaction of CCR4-NOT with EBF1 regulates gene-specific transcription and mRNA stability in B lymphopoiesis.Genes & development · 2016Article
- Transcriptional regulation of the proto-oncogene Zfp521 by SPI1 (PU.1) and HOXC13.Genesis (New York, N.Y. : 2000) · 2016Article
- Zfp521 promotes B-cell viability and cyclin D1 gene expression in a B cell culture system.Leukemia research · 2016Article
- Identification of cooperative genes for E2A-PBX1 to develop acute lymphoblastic leukemia.Cancer science · 2016Article
- ZNF423 and ZNF521: EBF1 Antagonists of Potential Relevance in B-Lymphoid Malignancies.BioMed research international · 2015Review
- Genetically engineered mouse models of human B-cell precursor leukemias.Cell cycle (Georgetown, Tex.) · 2014Review
- Coordinated transcriptional regulation of bone homeostasis by Ebf1 and Zfp521 in both mesenchymal and hematopoietic lineages.The Journal of experimental medicine · 2013Article
- Regulation of early adipose commitment by Zfp521.PLoS biology · 2012Article
- Acute lymphoblastic leukemia and developmental biology: a crucial interrelationship.Cell cycle (Georgetown, Tex.) · 2011Review
- Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia.Oncogene · 2010Article
- Altered metabolism and lipodystrophy in the early B-cell factor 1-deficient mouse.Endocrinology · 2010Article
- Gene profiling of the erythro- and megakaryoblastic leukaemias induced by the Graffi murine retrovirus.BMC medical genomics · 2010Article
- Emerging roles of the EBF family of transcription factors in tumor suppression.Molecular cancer research : MCR · 2009Review
- Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Article
- Article
- Zfp423 is required for normal cerebellar development.Molecular and cellular biology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Retroviral insertions that activate proto-oncogenes are a primary cause of tumors in certain strains of mice. The AKXD recombinant inbred mice are predisposed to a variety of leukemias and lymphomas as a result of viral integration. One common insertion site, the ecotropic viral insertion site 3 (Evi3), has been implicated in most B-cell tumors in the AKXD-27 strain. The Evi3 gene encodes a zinc-finger protein with sequence similarity to the Early B-cell Factor-Associated Zinc-finger gene (EBFAZ). We show that the Evi3 gene is overexpressed in several tumors with viral insertions at Evi3, which results in the upregulation of Early B-cell Factor (EBF)-target gene expression, suggesting that Evi3 modulates EBF activity. Reconstitution of primary leukemia cells showed that these tumors express high densities of the B-cell surface proteins CD19 and CD38, which are EBF targets. Using a transactivation assay, we show that the terminal six zinc-fingers of Evi3 are required for modification of EBF activity. This is the first evidence that Evi3 expression in tumors alters the level of EBF target genes, and the first characterization of the Evi3 protein domains required for modulation of EBF activity. Further, these data imply that Evi3 misexpression initiates tumorigenesis by perturbing B-cell development via an interaction with EBF.
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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.