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Analysis of Cell Type–specific Expression of CK1 in Various Tissues of Young Adult BALB/c Mice and in Mammary Tumors of SV40 T-Ag–transgenic Mice

Anja C. Utz, Heidrun Hirner, Annette Blatz, Andreas Hillenbrand, Bernhard Schmidt, Wolfgang Deppert, Doris Henne-Bruns, Dietmar Fischer, Dietmar R. Thal, Frank Leithäuser¹ and Uwe Knippschild¹

Departments of General, Visceral, and Transplantation Surgery (ACU,HH,AB,AH,BS,DH-B,UK), Experimental Neurology (DF), and Pathology (FL), and Laboratory of Neuropathology, Institute of Pathology (DRT), University of Ulm, Ulm, Germany, and Heinrich-Pette Institute for Experimental Immunology and Virology, University of Hamburg, Hamburg, Germany (WD)

Correspondence to: Uwe Knippschild, Department of General, Visceral, and Transplantation Surgery, University of Ulm, Steinhövelstr. 9, 89075, Ulm, Germany. E-mail: uwe.knippschild{at}uniklinik-ulm.de

Casein kinase 1 epsilon (CK1) is involved in various cellular processes, including cell growth, differentiation, and apoptosis, vesicle transport, and control of the circadian rhythm. Deregulation of CK1 has been linked to neurodegenerative diseases and cancer. To better understand the cell type–specific functions of CK1, we determined its localization by immunhistochemistry in tissues of healthy, young adult BALB/c mice and in mammary tumors of SV40 T-antigen–transgenic mice. CK1 expression was found to be highly regulated in normal tissues of endodermal, mesodermal, and ectodermal origin and in neoplastic tissue of mammary cancer. The data presented here give an overview of CK1 reactivity in different organs under normal conditions and outline changes in its expression in mammary carcinomas. Our data suggest a cell/organ type–specific function of CK1 and indicate that tumorigenic conversion of mammary glands in SV40 T-antigen–transgenic mice leads to downregulation of CK1. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials. (J Histochem Cytochem 58:1–15, 2010)

Key Words: CK1 • SV40 T-Ag–transgenic mice • mammary tumors • cell type–specific expression • signal transduction • immunohistochemistry

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