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Analysis of Cell Type-specific Expression of CK1ε in Various Tissues of Young Adult BALB/c Mice and in Mammary Tumors of SV40 T-Ag-transgenic Mice
Author(s) -
Anja C. Utz,
Heidrun Hirner,
Annette Blatz,
Andreas Hillenbrand,
Bernhard Schmidt,
Wolfgang Deppert,
Doris HenneBruns,
Dietmar Fischer,
Dietmar Rudolf Thal,
Frank Leithäuser,
Uwe Knippschild
Publication year - 2009
Publication title -
journal of histochemistry and cytochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.971
H-Index - 124
eISSN - 1551-5044
pISSN - 0022-1554
DOI - 10.1369/jhc.2009.954628
Subject(s) - biology , transgene , balb/c , genetically modified mouse , downregulation and upregulation , cell type , cell , antigen , cellular differentiation , cancer research , microbiology and biotechnology , pathology , immunology , immune system , gene , medicine , genetics
Casein kinase 1 epsilon (CK1epsilon) is involved in various cellular processes, including cell growth, differentiation, and apoptosis, vesicle transport, and control of the circadian rhythm. Deregulation of CK1epsilon has been linked to neurodegenerative diseases and cancer. To better understand the cell type-specific functions of CK1epsilon, 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. CK1epsilon 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 CK1epsilon 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 CK1epsilon and indicate that tumorigenic conversion of mammary glands in SV40 T-antigen-transgenic mice leads to downregulation of CK1epsilon. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

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