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Mojgan Djavaheri-Mergny

Researcher at University of Bordeaux

Publications -  65
Citations -  16720

Mojgan Djavaheri-Mergny is an academic researcher from University of Bordeaux. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 32, co-authored 62 publications receiving 14926 citations. Previous affiliations of Mojgan Djavaheri-Mergny include University of Paris & Curie Institute.

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PK11195 potently sensitizes to apoptosis induction independently from the peripheral benzodiazepin receptor.

TL;DR: In this paper, a model system was established in which PK11195 and another PBR ligand, 7-chloro-5-(4-chlorophenyl)-1,3-dihydro-1-methyl-2H-1,4-benzodiazepin-2-one (Ro5-4864), sensitize to nutrient depletion-induced cell death.
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Ultraviolet‐A induces activation of AP‐1 in cultured human keratinocytes

TL;DR: The finding suggests that UV‐A‐dependent AP‐1 activation is sensitive to the cellular redox state but is not related to membrane lipid peroxidation.
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2-Methoxyestradiol induces apoptosis in Ewing sarcoma cells through mitochondrial hydrogen peroxide production

TL;DR: Evidence is provided that 2-Me triggers apoptosis of Ewing sarcoma cells through induction of a mitochondria redox-dependent mechanism and it is suggested that this compound or other agents that selectively increase the level of reactive oxygen species may prove useful to the development of novel strategies for treatment of EWing tumors.
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c-Jun NH2-terminal kinase activation is essential for DRAM-dependent induction of autophagy and apoptosis in 2-methoxyestradiol-treated Ewing sarcoma cells.

TL;DR: Evidence is provided that 2-ME elicits macroautophagy, a process that participates in apoptotic responses, in a JNK-dependent manner, in Ewing sarcoma and osteosarcoma cells, and JNK is identified as a novel mediator of DRAM regulation.
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Apoptosis and autophagy have opposite roles on imatinib-induced K562 leukemia cell senescence

TL;DR: Interestingly, targeting autophagy by inhibiting ATG5 is accompanied by a strong SA-β-Gal staining, suggesting a specific inhibitory role on senescence, which is limiting the senescent response to imatinib, whereas Autophagy seems to have an opposite role.