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Sophie D. Lefevre

Researcher at University of Paris

Publications -  36
Citations -  1013

Sophie D. Lefevre is an academic researcher from University of Paris. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 15, co-authored 27 publications receiving 753 citations. Previous affiliations of Sophie D. Lefevre include Paris Diderot University & University of Groningen.

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From Erythroblasts to Mature Red Blood Cells: Organelle Clearance in Mammals.

TL;DR: Understanding the modulators of organelles clearance in erythropoiesis may elucidate the pathogenesis of different dyserythropOietic diseases such as myelodysplastic syndrome, leukemia and anemia.
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Friedreich Ataxia: Molecular Mechanisms, Redox Considerations, and Therapeutic Opportunities

TL;DR: The molecular mechanisms that underlie the disease phenotypes and the different hypothesis about the function of frataxin are highlighted and the most recent therapeutic approaches for this severe disease that actually has no efficient treatment are presented.
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The antifungal plant defensin RsAFP2 from radish induces apoptosis in a metacaspase independent way in Candida albicans

TL;DR: The data point to the existence of at least two different types of caspases or caspase‐like proteases in C. albicans, the first report on the induction of apoptosis with concomitant casp enzyme activation by a defensin in this pathogen.
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A biomimetic microfluidic chip to study the circulation and mechanical retention of red blood cells in the spleen.

TL;DR: A microfluidic chip successfully discriminated poorly deformable RBCs based on their distinct mechanical properties and on the intensity of the cell alteration to explore the exploration of the pathogenesis of malaria, hereditary spherocytosis, sickle cell disease and other RBC disorders are envisioned.
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Evidence that yeast frataxin is not an iron storage protein in vivo.

TL;DR: It is shown that large excesses of iron in the growth medium did not inhibit growth and did not decrease cell viability, and increasing the ratio of mitochondrial iron-to-Yfh1p by decreasing the steady-state level of Yfh2p to less than 100 molecules per cell had very few deleterious effects on cell physiology, even though the mitochondrial iron concentration greatly exceeded the iron-binding capacity of Y fh 1p in these conditions.