A5044366070- Cell death mechanisms and regulation
- Cancer Treatment and Pharmacology
- Cancer-related Molecular Pathways
- Microtubule and mitosis dynamics
- DNA Repair Mechanisms
- Cancer therapeutics and mechanisms
- Mitochondrial Function and Pathology
- Innovative Microfluidic and Catalytic Techniques Innovation
- PARP inhibition in cancer therapy
- Autophagy in Disease and Therapy
- HIV Research and Treatment
- RNA Interference and Gene Delivery
- Neuroscience and Neuropharmacology Research
- Endoplasmic Reticulum Stress and Disease
- CRISPR and Genetic Engineering
- Phagocytosis and Immune Regulation
- Drug Transport and Resistance Mechanisms
- Ubiquitin and proteasome pathways
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- ATP Synthase and ATPases Research
- Cancer, Hypoxia, and Metabolism
- interferon and immune responses
- RNA modifications and cancer
- Cancer Research and Treatments
Inserm
2013-2024
Centre de Recherche des Cordeliers
2014-2024
Université Paris Cité
2010-2024
Institut Universitaire de France
2024
Sorbonne Université
2015-2024
Institut Gustave Roussy
2011-2023
La Ligue Contre le Cancer
2014-2022
Sorbonne Paris Cité
2014-2018
Délégation Paris 5
2014-2018
Université Paris-Saclay
2007-2015
Programmed cell death (PCD) is a physiological process commonly defined by alterations in nuclear morphology (apoptosis) and/or characteristic stepwise degradation of chromosomal DNA occurring before cytolysis. However, determined characteristics PCD such as loss mitochondrial reductase activity or cytolysis can be induced enucleated cells, indicating cytoplasmic control. Here we report sequential disregulation function that precedes shrinkage and fragmentation. A first cyclosporin...
Anucleate cells can be induced to undergo programmed cell death (PCD), indicating the existence of a cytoplasmic PCD pathway that functions independently from nucleus. Cytoplasmic structures including mitochondria have been shown participate in control apoptotic nuclear disintegration. Before exhibit common signs apoptosis (chromatin condensation and endonuclease-mediated DNA fragmentation), they reduction mitochondrial transmembrane potential (delta psi m) may due opening permeability...
In a number of experimental systems in which lymphocyte depletion was induced by apoptosis-inducing manipulations, no apoptotic morphology and ladder-type DNA fragmentation were detected among freshly isolated peripheral lymphocytes ex vivo. Here we report that one alteration can be splenocytes stimulated with lymphocyte-depleting doses dexamethasone (DEX) vivo is reduced uptake 3,3'dihexyloxacarbocyanine iodide (DiOC6[3]), fluorochrome incorporates into cells dependent upon their...
Bcl-2 belongs to a family of apoptosis-regulatory proteins which incorporate into the outer mitochondrial as well nuclear membranes. The mechanism by proto-oncogene product inhibits apoptosis is thus far elusive. We and others have shown previously that first biochemical alteration detectable in cells undergoing apoptosis, before changes become manifest, collapse inner membrane potential (delta psi m), suggesting involvement products apoptotic cascade. Here we show mitochondria contain...
According to current understanding, cytoplasmic events including activation of protease cascades and mitochondrial permeability transition (PT) participate in the control nuclear apoptosis. However, relationship between PT has remained elusive. When apoptosis is induced by cross-linking Fas/APO-1/CD95 receptor, interleukin-1β converting enzyme (ICE; caspase 1) or ICE-like enzymes precedes disruption inner transmembrane potential (ΔΨm). In contrast, cytosolic CPP32/ Yama/Apopain/caspase 3...
In a number of experimental systems, the early stage apoptotic process, i.e. which precedes nuclear disintegration, is characterized by breakdown inner mitochondrial transmembrane potential ( ΔΨ m ). Here we address question as to whether permeability transition (PT) pores may account for dissipation in lymphocyte apoptosis. Drugs known their PT‐inhibitory (bongkrekic acid, cyclosporin A, and non‐immunosuppressive A analogue N ‐methyl‐Val‐4‐cyclosporin A) are capable preventing disruption....
Keeping Cancer Cells At Bay cells are often aneuploid; that is, they have an abnormal number of chromosomes. But to what extent this contributes the tumorigenic phenotype is not clear. Senovilla et al. (p. 1678 ; see Perspective by Zanetti and Mahadevan ) found tetraploidization cancer can cause them become immunogenic thus aid in their clearance from body immune system. with excess chromosomes put stress on endoplasmic reticulum, which leads movement protein calreticulin cell surface....
When cells undergo nuclear apoptosis (chromatin condensation, DNA fragmentation), they already manifest at least three alterations that can be quantified cytofluorometrically the single-cell level: 1) a loss of mitochondrial transmembrane potential (delta psi m), 2) an increased production superoxide anions, and 3) aberrant exposure phosphatidylserine (PS) residues on outer plasma membrane leaflet. This latter alteration allows for phagocytic recognition/elimination apoptotic cells. In this...
Abstract In a number of experimental systems, the early stage apoptotic process, i.e., that precedes nuclear disintegration, is characterized by breakdown inner mitochondrial transmembrane potential (delta psi(m)). This delta psi(m) disruption may involve permeability transition (PT). Here, we address question whether PT would suffice to cause apoptosis or, rather, it constitute secondary event not causally involved in cascade. Protoporphyrin IX (PPIX), ligand benzodiazepin receptor well...
Macroautophagy is known to participate in the quality control and turnover of cytoplasmic organelles, yet there little evidence that macroautophagy targets nuclei mammalian cells. Here, we investigated whether autophagy may target micronuclei, which arise as a result deficient bipolar chromosome segregation cells exposed cell cycle perturbations. After removal several distinct blockers (nocodazole, cytochalasin D, hydroxyurea or SP600125), manifested an increase frequency micronuclei...
Abstract Non–small cell lung carcinoma patients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses. Here, we show that PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant cancer cells distinct histologic origin. Cells manifesting elevated intracellular levels poly(ADP-ribosyl)ated proteins (PARhigh) responded to pharmacologic PARP inhibitors as well PARP1-targeting siRNAs by initiating DNA damage...