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Magnol, L.* ; Chevallier, M.C.* ; Nalesso, V.* ; Retif, S.* ; Fuchs, H. ; Klempt, M. ; Pereira, P.* ; Riottot, M.* ; Andrzejewski, S.* ; Doan, B.T.* ; Panthier, J.J.* ; Puech, A.* ; Beloeil, J.C.* ; Hrabě de Angelis, M. ; Herault, Y.*

KIT is required for hepatic function during mouse post-natal development.

BMC Dev. Biol. 7:81 (2007)
Publ. Version/Full Text Volltext DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Mouse phenotyping, systemic effects, lipid metabolism, Kit gene, hepatic function; COMBINED LIPASE DEFICIENCY; HEMATOPOIETIC STEM-CELLS; HIGH-DENSITY-LIPOPROTEIN; RECEPTOR-RELATED PROTEIN; SPOTTING W LOCUS; C-KIT; TYROSINE KINASE; GENE-EXPRESSION; FAT DIGESTION; ANIMAL-MODELS
e-ISSN 1471-213X
Journal BMC Developmental Biology
Quellenangaben Volume: 7, Issue: , Pages: , Article Number: 81 Supplement: ,
Publisher BioMed Central
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Experimental Genetics (IEG)