Loss of Memo, a novel FGFR regulator, results in reduced lifespan.

Détails

ID Serval
serval:BIB_92AB88B0676A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Loss of Memo, a novel FGFR regulator, results in reduced lifespan.
Périodique
Faseb Journal
Auteur(s)
Haenzi B., Bonny O., Masson R., Lienhard S., Dey J.H., Kuro-o M., Hynes N.E.
ISSN
1530-6860 (Electronic)
ISSN-L
0892-6638
Statut éditorial
Publié
Date de publication
01/2014
Peer-reviewed
Oui
Volume
28
Numéro
1
Pages
327-336
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
Memo is a widely expressed 33-kDa protein required for heregulin (HRG)-, epidermal growth factor (EGF)-, and fibroblast growth factor (FGF)-induced cell motility. Studies in mouse embryonic fibroblasts, wild-type or knockout for Memo, were performed to further investigate the role of Memo downstream of FGFR. We demonstrated that Memo associates with the FGFR signalosome and is necessary for optimal activation of signaling. To uncover Memo's physiological role, Memo conditional-knockout mice were generated. These animals showed a reduced life span, increased insulin sensitivity, small stature, graying hair, alopecia, kyphosis, loss of subcutaneous fat, and loss of spermatozoa in the epididymis. Memo-knockout mice also have elevated serum levels of active vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D), and calcium compared to control littermates expressing Memo. In summary, the results from in vivo and in vitro models support the hypothesis that Memo is a novel regulator of FGFR signaling with a role in controlling 1,25(OH)2D production and normal calcium homeostasis.
Mots-clé
Animals, Calcitriol/blood, Calcium/blood, Cells, Cultured, Immunohistochemistry, Immunoprecipitation, Mice, Nonheme Iron Proteins/genetics, Nonheme Iron Proteins/metabolism, Receptors, Fibroblast Growth Factor/metabolism, Vitamin D/blood
Pubmed
Web of science
Création de la notice
15/01/2015 15:05
Dernière modification de la notice
20/08/2019 14:55
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