Frédéric Dessauge
Pasteur Institute
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Featured researches published by Frédéric Dessauge.
Oncogene | 2005
Frédéric Dessauge; Sophia Hilaly; Martin Baumgartner; Brigitte Blumen; Dirk Werling; Gordon Langsley
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.
Biochimie | 2003
Gaël Roué; Natacha Bitton; Victor J. Yuste; Thomas Montange; Manuel Rubio; Frédéric Dessauge; Cécile Delettre; Hélène Merle-Béral; Marika Sarfati; Santos A. Susin
Ligation of CD47 by its natural ligand thrombospondin (TSP), or cross-linking by CD47 antibodies, triggers caspase-independent cell death in normal and leukemic cells. This kind of cell death is characterised by the cytoplasmic events of apoptosis including externalisation of phosphatidylserines and mitochondria swelling. We report herein selective mitochondrial changes in CD47-dependent cell death of T cells. After T cell stimulation via CD47, a rapid mitochondrial transmembrane potential (deltapsi(m)) disruption is accompanied by the production of reactive oxygen species (ROS) and phosphatidylserine exposure. Surprisingly, mitochondrial dysfunction does not induce cytochrome c or AIF release. Moreover, the dying cells do not exhibit caspase-3 activation and display intact nuclei without any large-scale, or oligonucleosomal DNA fragmentation. We conclude that DeltaPsi(m) loss and ROS production are an early step in CD47-dependent killing and neither cytochrome c, nor AIF are implicated in this new cell death pathway.
Biochimie | 2003
Alphonse Garcia; Xavier Cayla; Julien Guergnon; Frédéric Dessauge; Maria Paz Rebollo; Aarne Fleischer; Angelita Rebollo
Molecular Pharmacology | 2006
Julien Guergnon; Frédéric Dessauge; Victoria Dominguez; Jean P. Viallet; Serge Bonnefoy; Victor J. Yuste; Odile Mercereau-Puijalon; Xavier Cayla; Angelita Rebollo; Santos A. Susin; Pierre-Etienne Bost; Alphonse Garcia
Biochimie | 2003
Julien Guergnon; Frédéric Dessauge; Gordon Langsley; Alphonse Garcia
Molecular Cancer Research | 2004
Aarne Fleischer; Ata Ghadiri; Frédéric Dessauge; Marianne Duhamel; Xavier Cayla; Alphonse Garcia; Angelita Rebollo
Archive | 2003
Alphonse Garcia; Frédéric Dessauge; Gordon Langsley; Santos A. Susin; Xavier Cayla; Julien Guergnon; Angelita Rebollo
Archive | 2003
Alphonse Garcia; Frédéric Dessauge; Xavier Cayla; Angelita Rebollo
Archive | 2005
Alphonse Garcia; Frédéric Dessauge; Xavier Cayla; Angelita Rebollo
Archive | 2003
Alphonse Garcia; Frédéric Dessauge; Gordon Langsley; Santos A. Susin; Xavier Cayla; Julien Guergnon; Angelita Rebollo