KIT is required for hepatic function during mouse post-natal development.
Fiche publication
Date publication
juillet 2007
Journal
BMC developmental biology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr HERAULT Yann
Tous les auteurs :
Magnol L, Chevallier MC, Nalesso V, Retif S, Fuchs H, Klempt M, Pereira P, Riottot M, Andrzejewski S, Doan BT, Panthier JJ, Puech A, Beloeil JC, de Angelis MH, Hérault Y
Lien Pubmed
Résumé
The Kit gene encodes a receptor tyrosine kinase involved in various biological processes including melanogenesis, hematopoiesis and gametogenesis in mice and human. A large number of Kit mutants has been described so far showing the pleiotropic phenotypes associated with partial loss-of-function of the gene. Hypomorphic mutations can induce a light coat color phenotype while complete lack of KIT function interferes with embryogenesis. Interestingly several intermediate hypomorphic mutations induced in addition growth retardation and post-natal mortality.
Mots clés
Alleles, Anemia, genetics, Animals, Animals, Newborn, Fatty Liver, genetics, Fetal Stem Cells, metabolism, Gene Expression Regulation, Developmental, Lipid Metabolism, genetics, Liver, embryology, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Mutation, Phenotype, Proto-Oncogene Proteins c-kit, genetics, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction
Référence
BMC Dev. Biol.. 2007 Jul;7:81