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X-WR-CALDESC:Institut de génomique fonctionnelle
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DTSTART:20261025T020000
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UID:MEC-836a0dcbf5d22652569dc3a708274c16@igf.cnrs.fr
DTSTART;TZID=Europe/Paris:20261106T080000
DTEND;TZID=Europe/Paris:20261106T090000
DTSTAMP:20261012T105453Z
CREATED:20261012
LAST-MODIFIED:20261012
PRIORITY:5
SEQUENCE:5
TRANSP:OPAQUE
SUMMARY:Thesis – Clémence ROUÉ
DESCRIPTION:Deciphering ADAM10 function in node of Ranvier establishment and in autoimmune nodopathy\nJury\n\nLaurence GOUTEBROZE, Research Director, Institut de Biologie Paris-Seine, Paris – Reviewer\nAnne-Sophie LIA, Assistant Professor-Hospital Physician, Institut OmegaHealth, Limoges – Reviewer\nAnne DESMAZIERES, Research scientist, Paris Brain Institute – Examiner\nCharbel MASSAAD, Professor, Université Paris Cité – Examiner\nAlexandre JENTZER, Professor-Hospital Physician, IGF, Université de Montpellier – co-supervisor\nJérôme DEVAUX, Research Director, IGF, University of Montpellier – Thesis supervisor\n\n \nSummary\nNeurofascin-155 (Nfasc155) is a cell adhesion protein that plays an important role in the formation of node of Ranvier and the maintenance of saltatory conduction. Nfasc155 is targeted by autoantibodies in autoimmune nodopathy, leading to motor and sensory deficits. We recently discovered that ADAM10, a metalloprotease, is expressed at the node of Ranvier. We sought to determine whether ADAM10 contributes to the formation of the node of Ranvier by cleaving nodal and paranodal proteins. We demonstrated that Nfasc155 is cleaved by ADAM10 in myelinating glial cells ex vivo. Since the degradation of Nfasc155 appears to be responsible for the paranodal alterations observed in autoimmune nodopathy, we demonstrated the involvement of ADAM10 in the pathophysiology of autoimmune nodopathy in vivo.\n
URL:https://www.igf.cnrs.fr/en/events/thesis-clemence-roue/
CATEGORIES:Thesis
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