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- Title
c-Myc activation by Theileria parasites promotes survival of infected B-lymphocytes.
- Authors
Dessauge, Frédéric; Hilaly, Sophia; Baumgartner, Martin; Blumen, Brigitte; Werling, Dirk; Langsley, Gordon
- Abstract
THEILERIA: parasites infect and transform bovine lymphocytes, but host cell immortalization is reversible, as upon parasite death the lymphocytes rapidly die of apoptosis. Infection leads to a marked augmentation in the levels of lymphocyte c-Myc, and the parasite achieves this by inducing increased c-myc transcription and by prolonging the half-life of the transcription factor. Reduction in c-Myc turnover can be ascribed to CK2-mediated phosphorylation of the transcription factor. A parasite-dependent GM-CSF autocrine loop activates a JAK2/STAT3 signalling pathway that contributes to heightened c-myc transcription, and inhibition of the pathway leads to caspase 9 activation and apoptosis that can be directly ascribed to a reduction in c-Myc. An antiapoptotic role for c-Myc was clearly demonstrated by specific inhibition of c-myc expression with antisense oligonucleotides, and this correlates with loss of the antiapoptotic protein Mcl-1, and, consistently, ectopic expression of c-Myc abrogates B-cell death induced upon JAK2 inhibition. Thus, Theileria parasites ensure the survival of their host lymphocytes via specific activation of c-Myc.Oncogene (2005) 24, 1075-1083. doi:10.1038/sj.onc.1208314 Published online 6 December 2004
- Subjects
DEATH (Biology); TRANSCRIPTION factors; APOPTOSIS; PROTEINS; CELL death; HELIX-loop-helix motifs
- Publication
Oncogene, 2005, Vol 24, Issue 6, p1075
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/sj.onc.1208314