Abstract
Theileria parasitises bovine leukocytes and transforms them into proliferating, metastatic tumours, where the infection resembles a leukaemia-like disease. We have studied the signal transduction pathways leading to activation of the transcription factor AP-1 in different transformed leukocytes. Parasite infection leads to an up-regulation of all members of the Jun/Fos family of proteins and surprisingly, this occurs in the absence of any detectable ERK, or p38 MAP kinase activity. In the parasitised B-sarcoma TBL3, AP-1 induction occurs in the absence of any JNK activity. In contrast, in infected macrophage and B-cell lines, AP-1 transcriptional activity is strictly associated with the parasite-induced constitutive activation of JNK and subsequent c-Jun N-terminal phosphorylation. Thus, constant AP-1 transcriptional activity involves both an upregulation in the levels of Jun and Fos proteins and constitutive JNK activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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B-Lymphocytes / enzymology
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B-Lymphocytes / parasitology
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cattle
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Cells, Cultured
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Enzyme Activation
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Gene Expression Regulation, Enzymologic
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JNK Mitogen-Activated Protein Kinases
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Leukocytes / enzymology
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Leukocytes / metabolism
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Leukocytes / parasitology*
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Lymphocyte Activation
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Macrophages / enzymology
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Macrophages / parasitology
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Mitogen-Activated Protein Kinases*
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Phosphorylation
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Proto-Oncogene Proteins c-fos / metabolism*
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Proto-Oncogene Proteins c-jun / metabolism*
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Signal Transduction
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Theileria / genetics
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Theileria / physiology*
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Transcription Factor AP-1 / metabolism*
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Transcriptional Activation
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Tumor Cells, Cultured
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Up-Regulation
Substances
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Proto-Oncogene Proteins c-fos
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Proto-Oncogene Proteins c-jun
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Transcription Factor AP-1
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Calcium-Calmodulin-Dependent Protein Kinases
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases