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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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Identification of two human nuclear proteins that recognise the cytosine-rich strand of human telomeres in vitro.

TL;DR: Several nuclear factors from human cell extracts are isolated that specifically bind the C-rich strand of vertebrate telomeres with high affinity and bind double-stranded telomere cytosine-rich (C-rich) strand with 100xreduced affinity.
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Regulation of autophagy by NFkappaB transcription factor and reactives oxygen species.

TL;DR: Evidence is brought that direct stimulation of autophagy may represent a new therapeutic strategy for overcoming the NF-κappaB-dependent chemoresistance of cancer cells and support the idea that repression ofAutophagy by NF-kappaB may constitute a novel anti-apoptotic function of this transcription factor.
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Glutaminolysis and autophagy in cancer.

TL;DR: A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies.
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Autophagosome maturation is impaired in Fabry disease

TL;DR: Findings suggest that Fabry disease is linked to a deregulation of autophagy, with increased basal levels compared to cells from non-Fabry subjects and a larger increase in response to starvation than seen in non- Fabry cells.
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Oxidized low density lipoprotein induces activation of the transcription factor NFκB in fibroblasts, endothelial and smooth muscle cells

TL;DR: The study supports the evidence that the stress induced by oxidized LDL causes NFκB activation in different cell types, and that this effect can be ascribed to the lipid peroxidation products.