G
Guido Kroemer
Researcher at Institut Gustave Roussy
Publications - 1546
Citations - 294816
Guido Kroemer is an academic researcher from Institut Gustave Roussy. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 236, co-authored 1404 publications receiving 246571 citations. Previous affiliations of Guido Kroemer include Karolinska Institutet & Spanish National Research Council.
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DRAM: a phylogenetically ancient regulator of autophagy.
TL;DR: Analysis of DRAM-related proteins reveals evolutionarily conserved and divergent roles in the control of autophagy.
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OncoImmunology: a new journal at the frontier between oncology and immunology
Laurence Zitvogel,Guido Kroemer +1 more
TL;DR: The last two years confirmed the research-based hypothesis that chemotherapy must stimulate an anticancer immune response in order to be successful and marked a turning point in the field.
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Aspirin—another caloric-restriction mimetic
TL;DR: It is found that the ancient drug aspirin and its active metabolite salicylate stimulate autophagic flux by virtue of their inhibitory action on acetyltransferase EP300, and acts as a Caloric-restriction mimetics (CRM) that recapitulate the main biochemical properties of CR.
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The oncolytic compound LTX-401 targets the Golgi apparatus
Heng Zhou,Allan Sauvat,Lígia C. Gomes-da-Silva,Sylvère Durand,Sabrina Forveille,Kristina Iribarren,Takahiro Yamazaki,Sylvie Souquere,Lucillia Bezu,Kevin Müller,Marion Leduc,Peng Liu,Liwei Zhao,Aurélien Marabelle,Laurence Zitvogel,Øystein Rekdal,Oliver Kepp,Guido Kroemer +17 more
TL;DR: The contention that LTX-401 can stimulate immunogenic cell death through a pathway in which Golgi-localized L TX-401 operates upstream of mitochondrial membrane permeabilization is supported.
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Cd69-induced monocyte apoptosis involves multiple nonredundant signaling pathways
TL;DR: In conclusion, simultaneous stimulation of human monocytes/macrophages or THP1 cells with LPS and an antibody specific for the activation marker CD69 induces apoptosis and the involvement of multiple independent signals that are necessary for apoptosis induction is demonstrated.