Fiche publication
Date publication
août 1996
Journal
Proceedings of the National Academy of Sciences of the United States of America
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre
,
Dr KASTNER Philippe
,
Dr MARK Manuel
,
Dr KREZEL Wojciech
Tous les auteurs :
Krezel W, Dupé V, Mark M, Dierich A, Kastner P, Chambon P
Lien Pubmed
Résumé
The RXR gamma (RXR, retinoid X receptor) gene was disrupted in the mouse. Homozygous mutant mice developed normally and were indistinguishable from their RXR gamma +/- or wild-type littermates with respect to growth, fertility, viability, and apparent behavior in the animal facility. Moreover, RXR alpha -/-/RXR gamma -/- and RXR beta -/-/RXR gamma -/- mutant phenotypes were indistinguishable from those of RXR alpha -/- and RXR beta -/- mutants, respectively. Strikingly, RXR alpha +/-/RXR beta -/-/RXR gamma -/- triple mutants were viable. Thus, it appears that RXR gamma does not exert any essential function that cannot be performed by RXR alpha or RXR beta, and one copy of RXR alpha is sufficient to perform most of the functions of the RXRs.
Mots clés
Animals, Body Weight, Heterozygote, Homozygote, Mice, Mice, Knockout, embryology, Molecular Sequence Data, Muscle Development, Muscle, Skeletal, chemistry, RNA, Messenger, isolation & purification, Receptors, Retinoic Acid, genetics, Retinoid X Receptors, Tissue Distribution, Transcription Factors, genetics
Référence
Proc. Natl. Acad. Sci. U.S.A.. 1996 Aug;93(17):9010-4
