Chloé Borde
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Chloé Borde has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Alexandre E. Escargueil
Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, F-75012, Paris, France
1 shared publication Bharath Wootla
Office of Translation to Practice, Center for Clinical and Translational Science (CCaTS), Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
1 shared publication- Frédérique Quignon
Sorbonne Université, CNRS UMR 144, Institut Curie Centre de Recherche, F-75248 Paris, France
1 shared publication Lakhdar Fattoum
Sorbonne Université, INSERM, Laboratory of Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine (CRSA), F-75012 Paris, France
1 shared publicationSrini Kaveri
INSERM UMRS 1138, Centre de Recherche des Cordeliers, Paris, France
1 shared publicationStéphanie Barnay-Verdier
Sorbonne Université, Paris, France; CNRS, INSERM, Université Côte d'Azur, Institute for Research on Cancer and Aging, Nice, France
1 shared publication
Latest Publications
- 1 January 2020
- Published by Elsevier in Cellular Immunology
- Vol. 347, 104020
Emergence of antibodies endowed with proteolytic activity against High-mobility group box 1 protein (HMGB1) in patients surviving septic shock
- 1 January 2020
- Published by Elsevier in Cellular Immunology
- Vol. 347, 104020
Emergence of antibodies endowed with proteolytic activity against High-mobility group box 1 protein (HMGB1) in patients surviving septic shock
- Open Access
Epstein–Barr Virus BALF0 and BALF1 Modulate Autophagy
Autophagy is an essential catabolic process that degrades cytoplasmic components within the lysosome, therefore ensuring cell survival and homeostasis. A growing number of viruses, including members of the Herpesviridae family, have been shown to manipulate autophagy to facilitate their persistence or optimize their replication. Previous works showed that the Epstein–Barr virus (EBV), a human transforming gammaherpesvirus, hijacked autophagy during the lytic phase of its cycle, possibly to favor the formation of viral particles. However, the viral proteins that are responsible for an EBV-mediated subversion of the autophagy pathways remain to be characterized. Here we provide the first evidence that the BALF0/1 open reading frame encodes for two conserved proteins of the Bcl-2 family, BALF0 and BALF1, that are expressed during the early phase of the lytic cycle and can modulate autophagy. A putative LC3-interacting region (LIR) has been identified that is required both for BALF1 colocalization with autophagosomes and for its ability to stimulate autophagy.
Open AccessEpstein–Barr Virus BALF0 and BALF1 Modulate Autophagy
Autophagy is an essential catabolic process that degrades cytoplasmic components within the lysosome, therefore ensuring cell survival and homeostasis. A growing number of viruses, including members of the Herpesviridae family, have been shown to manipulate autophagy to facilitate their persistence or optimize their replication. Previous works showed that the Epstein–Barr virus (EBV), a human transforming gammaherpesvirus, hijacked autophagy during the lytic phase of its cycle, possibly to favor the formation of viral particles. However, the viral proteins that are responsible for an EBV-mediated subversion of the autophagy pathways remain to be characterized. Here we provide the first evidence that the BALF0/1 open reading frame encodes for two conserved proteins of the Bcl-2 family, BALF0 and BALF1, that are expressed during the early phase of the lytic cycle and can modulate autophagy. A putative LC3-interacting region (LIR) has been identified that is required both for BALF1 colocalization with autophagosomes and for its ability to stimulate autophagy.