J
Jean-Marie Naeyaert
Researcher at Ghent University Hospital
Publications - 30
Citations - 2451
Jean-Marie Naeyaert is an academic researcher from Ghent University Hospital. The author has contributed to research in topics: Vitiligo & Cutis laxa. The author has an hindex of 21, co-authored 30 publications receiving 2327 citations. Previous affiliations of Jean-Marie Naeyaert include Ghent University.
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Journal ArticleDOI
Evidence for an Autoimmune Pathogenesis of Vitiligo
TL;DR: A variety of arguments from clinical observations to research findings in human and animal models support the hypothesis of autoimmunity, and new insights in the association of vitiligo and melanoma may help to clarify the role of autoIMmunity in the development of Vitiligo.
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Loss-of-function mutations in LEMD3 result in osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis.
Jan Hellemans,Olena Preobrazhenska,Andy Willaert,Philippe Debeer,Peter Verdonk,Teresa Costa,Katrien Janssens,Björn Menten,Nadine Van Roy,Stefan Vermeulen,Ravi Savarirayan,Wim Van Hul,Filip Vanhoenacker,Danny Huylebroeck,Anne De Paepe,Jean-Marie Naeyaert,Jo Vandesompele,Frank Speleman,Kristin Verschueren,Paul Coucke,Geert Mortier +20 more
TL;DR: In this study, LEMD3 interacted with BMP and activin-TGFβ receptor–activated Smads and antagonized both signaling pathways in human cells and interacted with XMAN1, the Xenopus laevis ortholog, which antagonizes BMP signaling during embryogenesis.
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Homozygosity for a missense mutation in fibulin-5 (FBLN5) results in a severe form of cutis laxa
Bart Loeys,Lionel Van Maldergem,Geert Mortier,Paul Coucke,Sabine Gerniers,Jean-Marie Naeyaert,Anne De Paepe +6 more
TL;DR: Evidence is provided that a genetic defect in fibulin-5 (FBLN5, also known as EVEC or DANCE) is responsible for a recessive form of cutis laxa in humans.
Journal ArticleDOI
The quest for the mechanism of melanin transfer.
TL;DR: A central role has been established for the protease‐activated receptor‐2 of the keratinocyte which effectuates melanin transfer via phagocytosis, and clues as to what mechanism and molecular machinery will arise with the identification of the function of specific genes which are mutated in diseases that affect transfer are being identified.
Book Chapter
Hypomelanoses and hypermelanoses
Hilde Lapeere,Barbara Boone,Sofie De Schepper,Evelien Verhaeghe,Katia Ongenae,Nanja van Geel,Jo Lambert,Lieve Brochez,Jean-Marie Naeyaert +8 more
TL;DR: The Griscelli syndrome presents in accelerated phase with neurological involvement and the role of mutations in the RAB27A gene as an indication for BMT is unclear.