S
Stéphane Emiliani
Researcher at French Institute of Health and Medical Research
Publications - 67
Citations - 8565
Stéphane Emiliani is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Integrase & Viral replication. The author has an hindex of 34, co-authored 60 publications receiving 8103 citations. Previous affiliations of Stéphane Emiliani include Paris Descartes University & Institut Gustave Roussy.
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SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx
Nadine Laguette,Bijan Sobhian,Nicoletta Casartelli,Mathieu Ringeard,Christine Chable-Bessia,Emmanuel Ségéral,Ahmad Yatim,Stéphane Emiliani,Olivier Schwartz,Monsef Benkirane +9 more
TL;DR: It is demonstrated that SAMHD1 is an antiretroviral protein expressed in cells of the myeloid lineage that inhibits an early step of the viral life cycle, and is probably required for HIV-1 restriction.
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A class of hybrid polar inducers of transformed cell differentiation inhibits histone deacetylases
Victoria M. Richon,Stéphane Emiliani,Eric Verdin,Yael Webb,Ronald Breslow,Richard A. Rifkind,Paul A. Marks +6 more
TL;DR: These studies show that the second-generation HPCs, unlike HMBA, are potent inhibitors of HDAC activity, and appear to induce differentiation by different pathways.
Journal Article
The expression of a small fraction of cellular genes is changed in response to histone hyperacetylation.
TL;DR: It is demonstrated that the transcriptional regulation of a restricted set of cellular genes is uniquely sensitive to the degree of histone acetylation in chromatin, and two new specific inhibitors of hist one deacetylase are used.
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Transcriptional activation and chromatin remodeling of the HIV-1 promoter in response to histone acetylation.
TL;DR: Chromatin analysis of the HIV‐1 genome shows that a single nucleosome (nuc‐1) located at the transcription start and known to be disrupted following TNF‐alpha treatment, is also disrupted following TPX or TSA treatment, demonstrating that transcriptional activation of HIV‐ 1 can proceed through a chromatin modification.
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Post-activation Turn-off of NF-κB-dependent Transcription Is Regulated by Acetylation of p65
Rosemary Kiernan,Vanessa Brès,Raymond W. M. Ng,Marie-Pierre Coudart,Selma El Messaoudi,Claude Sardet,Dong-Yan Jin,Stéphane Emiliani,Monsef Benkirane +8 more
TL;DR: This work shows that the p65 subunit of NF-κB is acetylated by both p300 and PCAF on lysines 122 and 123 and proposes that acetylation of p65 plays a key role in IκΒα-mediated attenuation ofNF-κΓ transcriptional activity which is an important process that restores the latent state in post-induced cells.