ZNF423 and ZNF521: EBF1 Antagonists of Potential Relevance in B-Lymphoid Malignancies.
Maria Mesuraca, Emanuela Chiarella, Stefania Scicchitano, Bruna Codispoti, Marco Giordano, Giovanna Nappo, Heather M Bond, Giovanni Morrone
Journal: BioMed research international
2016;2015():165238
PMID: 26788497
Abstract
["The development of the B-lymphoid cell lineage is tightly controlled by the concerted action of a network of transcriptional and epigenetic regulators. EBF1, a central component of this network, is essential for B-lymphoid specification and commitment as well as for the maintenance of the B-cell identity. Genetic alterations causing loss of function of these B-lymphopoiesis regulators have been implicated in the pathogenesis of B-lymphoid malignancies, with particular regard to B-cell acute lymphoblastic leukaemias (B-ALLs), where their presence is frequently detected. The activity of the B-cell regulatory network may also be disrupted by the aberrant expression of inhibitory molecules. In particular, two multi-zinc finger transcription cofactors named ZNF423 and ZNF521 have been characterised as potent inhibitors of EBF1 and are emerging as potentially relevant contributors to the development of B-cell leukaemias. Here we will briefly review the current knowledge of these factors and discuss the importance of their functional cross talk with EBF1 in the development of B-cell malignancies."]
Address:
Laboratory of Molecular Haematopoiesis and Stem Cell Biology, Department of Experimental and Clinical Medicine, Magna Græcia University, 88100 Catanzaro, Italy.; Laboratory of Molecular Haematopoiesis and Stem Cell Biology, Department of Experimental and Clinical Medicine, Magna Græcia University, 88100 Catanzaro, Italy; YCR Cancer Research Unit, Department of Biology, University of York, Heslington, York YO10 5DD, UK.
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MeSH Terms:
Cell Lineage,
DNA-Binding Proteins,
Gene Expression Regulation, Leukemic,
Gene Regulatory Networks,
Humans,
Lymphopoiesis,
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,
Proteins,
Signal Transduction,
Trans-Activators