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Fabrice P. Cordelières

Researcher at French Institute of Health and Medical Research

Publications -  36
Citations -  10155

Fabrice P. Cordelières is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: DNA repair & Microscope. The author has an hindex of 19, co-authored 32 publications receiving 8821 citations. Previous affiliations of Fabrice P. Cordelières include Centre national de la recherche scientifique & Curie Institute.

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Journal ArticleDOI

A guided tour into subcellular colocalization analysis in light microscopy

TL;DR: A novel toolbox for subcellular colocalization analysis under ImageJ is created that integrates current global statistic methods and a novel object‐based approach to assess proteins residing on intracellular structures by fluorescence microscopy.
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BoneJ: Free and extensible bone image analysis in ImageJ.

TL;DR: This work implemented standard bone measurements in a novel ImageJ plugin, BoneJ, with which it analysed trabecular bone, whole bones and osteocyte lacunae and found that available software solutions were expensive, inflexible or methodologically opaque.
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Huntingtin Controls Neurotrophic Support and Survival of Neurons by Enhancing BDNF Vesicular Transport along Microtubules

TL;DR: It is shown that huntingtin specifically enhances vesicular transport of brain-derived neurotrophic factor (BDNF) along microtubules, indicating that a key role of huntingtin is to promote BDNF transport and suggesting that loss of this function might contribute to pathogenesis.
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Histone Deacetylase 6 Inhibition Compensates for the Transport Deficit in Huntington's Disease by Increasing Tubulin Acetylation

TL;DR: It is reported here that HDAC inhibitors, including trichostatin A (TSA), increase vesicular transport of brain-derived neurotrophic factor (BDNF) by inhibiting HDAC6, thereby increasing acetylation at lysine 40 of α-tubulin.
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The IGF-1/Akt Pathway Is Neuroprotective in Huntington's Disease and Involves Huntingtin Phosphorylation by Akt

TL;DR: It is demonstrated that huntingtin is a substrate of Akt and that phosphorylation of huntingtin by Akt is crucial to mediate the neuroprotective effects of IGF-1 and it is shown that AkT is altered in Huntington's disease patients.