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Constitutively activated CK2 potentially plays a pivotal role in Theileria-induced lymphocyte transformation

Published online by Cambridge University Press:  11 November 2005

F. DESSAUGE
Affiliation:
Laboratoire de Biologie Cellulaire Comparative des Apicomplexes, UMR 8104 CNRS/U567 INSERM, Département Maladies Infectieuses, Hôpital Cochin – Bâtiment Gustave Roussy, Institut Cochin, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France Laboratoire d'Immunologie Cellulaire et Tissulaire, INSERM U543, Bâtiment CERVI Groupe Hospitalier Pitié-Salpêtrière, 83, Boulevard de l'Hôpital, 75651 Paris Cedex 13 France
R. LIZUNDIA
Affiliation:
Laboratoire de Biologie Cellulaire Comparative des Apicomplexes, UMR 8104 CNRS/U567 INSERM, Département Maladies Infectieuses, Hôpital Cochin – Bâtiment Gustave Roussy, Institut Cochin, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France
G. LANGSLEY
Affiliation:
Laboratoire de Biologie Cellulaire Comparative des Apicomplexes, UMR 8104 CNRS/U567 INSERM, Département Maladies Infectieuses, Hôpital Cochin – Bâtiment Gustave Roussy, Institut Cochin, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France

Abstract

Activation of casein kinase II (CK2) was one of the first observations made on how Theileria parasites manipulate host cell signal transduction pathways and we argue that CK2 induction may in fact contribute to many of the different activation events that have been described since 1993 for Theileria-infected lymphocytes such as sustained activation of transcription factors c-Myc and NF-κB. CK2 also contributes to infected lymphocyte survival by inhibiting caspase activation and is probably behind constitutive PI3-K activation by phosphorylating PTEN. Finally, we also discuss how CK2A may act not only as a kinase, but also as a stimulatory subunit for the protein phosphatase PP2A, so dampening down the MEK/ERK and Akt/PKB pathways and for all these reasons we propose CK2 as a central player in Theileria-induced lymphocyte transformation.

Type
Research Article
Copyright
© 2005 Cambridge University Press

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