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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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A fluorescence-microscopic and cytofluorometric system for monitoring the turnover of the autophagic substrate p62/SQSTM1.

TL;DR: It is demonstrated that a HaloTag®-p62 fusion protein stably expressed in suitable cell lines can be used to monitor autophagy by flow cytometry and automated fluorescence microscopy and it is surmised that this system could be adapted to high-throughput applications.
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Therapy-induced tumor immunosurveillance involves IFN-producing killer dendritic cells.

TL;DR: A unique class of IFN-producing killer dendritic cells resembling natural killer cells has been defined that can recognize and lyse tumor cells through a tumor necrosis factor-related apoptosis-inducing ligand-dependent mechanism.
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Mechanisms of p53-mediated mitochondrial membrane permeabilization.

TL;DR: This data indicates that the number of cells in the Tournais-Sud XI region is connected to the Toulonian immune system through a Tournai-like process called “cell reprograming”, which results in down-regulation in the immune defences of the immune system.
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Suppression of tumor antigen presentation during aneuploid tumor evolution contributes to immune evasion.

TL;DR: Using a mouse model of the in vivo evolution of aneuploid tumors, it is found that the induction of chromosomal instability in tumor cells is highly immunogenic due to the activation of the STING/TBK1 pathway and consequent increased interferon signaling and antigen presentation.
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La catastrophe mitotique : un cas particulier d'apoptose

TL;DR: A molecular pathway through which failure to arrest the cell cycle and inhibition of apoptosis can favor the occurrence of cytogenetic abnormalities which are likely to participate in oncogenesis is delineated.