Deficient T cell fate specification in mice with an induced inactivation of Notch1.

Détails

ID Serval
serval:BIB_2776E07ECD34
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Deficient T cell fate specification in mice with an induced inactivation of Notch1.
Périodique
Immunity
Auteur(s)
Radtke F., Wilson A., Stark G., Bauer M., van Meerwijk J., MacDonald H.R., Aguet M.
ISSN
1074-7613 (Print)
ISSN-L
1074-7613
Statut éditorial
Publié
Date de publication
1999
Peer-reviewed
Oui
Volume
10
Numéro
5
Pages
547-558
Langue
anglais
Résumé
Notch proteins are cell surface receptors that mediate developmental cell specification events. To explore the function of murine Notch1, an essential portion of the gene was flanked with loxP sites and inactivation induced via interferon-regulated Cre recombinase. Mice with a neonatally induced loss of Notch1 function were transiently growth retarded and had a severe deficiency in thymocyte development. Competitive repopulation of lethally irradiated wild-type hosts with wild-type- and Notch1-deficient bone marrow revealed a cell autonomous blockage in T cell development at an early stage, before expression of T cell lineage markers. Notch1-deficient bone marrow did, however, contribute normally to all other hematopoietic lineages. These findings suggest that Notch1 plays an obligatory and selective role in T cell lineage induction.
Mots-clé
Animals, Animals, Newborn, Antigens, CD4/genetics, Antigens, CD8/genetics, B-Lymphocytes/cytology, Cell Differentiation/drug effects, Cell Division/genetics, Flow Cytometry, Gene Expression, Gene Expression Regulation, Membrane Proteins/genetics, Mice, Mice, Transgenic, Phenotype, Receptor, Notch1, Receptors, Cell Surface, T-Lymphocytes/cytology, Thymus Gland/growth & development, Transcription Factors
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 11:39
Dernière modification de la notice
20/08/2019 13:06
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