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Protein signaling and regulation of gene transcription in leukemia: role of the Casein Kinase II-Ikaros axis

Chandrika S Gowda, Chunhua Song, Yali Ding, Malika Kapadia, Sinisa Dovat
DOI: 10.1136/jim-2016-000075 Published 24 February 2016
Chandrika S Gowda
Department of Pediatrics, Penn State University College of Medicine, Hershey, Pennsylvania, USA
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Chunhua Song
Department of Pediatrics, Penn State University College of Medicine, Hershey, Pennsylvania, USA
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Yali Ding
Department of Pediatrics, Penn State University College of Medicine, Hershey, Pennsylvania, USA
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Malika Kapadia
Department of Pediatrics, Penn State University College of Medicine, Hershey, Pennsylvania, USA
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Sinisa Dovat
Department of Pediatrics, Penn State University College of Medicine, Hershey, Pennsylvania, USA
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Abstract

Protein signaling and regulation of gene expression are the two major mechanisms that regulate cellular proliferation in leukemia. Discerning the function of these processes is essential for understanding the pathogenesis of leukemia and for developing the targeted therapies. Here, we provide an overview of one of the mechanisms that regulates gene transcription in leukemia. This mechanism involves the direct interaction between Casein Kinase II (CK2) and the Ikaros transcription factor. Ikaros (IKZF1) functions as a master regulator of hematopoiesis and a tumor suppressor in acute lymphoblastic leukemia (ALL). Impaired Ikaros function results in the development of high-risk leukemia. Ikaros binds to the upstream regulatory elements of its target genes and regulates their transcription via chromatin remodeling. In vivo, Ikaros is a target for CK2, a pro-oncogenic kinase. CK2 directly phosphorylates Ikaros at multiple amino acids. Functional experiments showed that CK2-mediated phosphorylation of Ikaros, regulates Ikaros’ DNA binding affinity, subcellular localization and protein stability. Recent studies revealed that phosphorylation of Ikaros by CK2 regulates Ikaros binding and repression of the terminal deoxytransferase (TdT) gene in normal thymocytes and in T-cell ALL. Available data suggest that the oncogenic activity of CK2 in leukemia involves functional inactivation of Ikaros and provide a rationale for CK2 inhibitors as a potential treatment for ALL.

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Vol 64 Issue 3 Table of Contents
Journal of Investigative Medicine: 64 (3)
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Protein signaling and regulation of gene transcription in leukemia: role of the Casein Kinase II-Ikaros axis
Chandrika S Gowda, Chunhua Song, Yali Ding, Malika Kapadia, Sinisa Dovat
Journal of Investigative Medicine Mar 2016, 64 (3) 735-739; DOI: 10.1136/jim-2016-000075

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Protein signaling and regulation of gene transcription in leukemia: role of the Casein Kinase II-Ikaros axis
Chandrika S Gowda, Chunhua Song, Yali Ding, Malika Kapadia, Sinisa Dovat
Journal of Investigative Medicine Mar 2016, 64 (3) 735-739; DOI: 10.1136/jim-2016-000075
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Protein signaling and regulation of gene transcription in leukemia: role of the Casein Kinase II-Ikaros axis
Chandrika S Gowda, Chunhua Song, Yali Ding, Malika Kapadia, Sinisa Dovat
Journal of Investigative Medicine Mar 2016, 64 (3) 735-739; DOI: 10.1136/jim-2016-000075
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  • Article
    • Abstract
    • Introduction
    • Structure and biologic function of Ikaros
    • Role of Ikaros as a tumor suppressor in leukemia
    • Phosphorylation of Ikaros by CK2 controls Ikaros activity
    • Dephosphorylation of Ikaros by protein phosphatase 1
    • Phosphorylation regulates stability of Ikaros protein
    • CK2 and PP1 Regulate Ikaros-mediated repression of TdT and cellular proliferation in leukemia
    • Targeting CK2-Ikaros pathway in B cell Leukemia
    • Conclusion
    • Acknowledgments
    • Footnotes
    • References
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