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Reversible and tissue-specific activation of MAP kinase signaling by tamoxifen in brafV637 ERT2 mice.

Genesis 51, 448-455 (2013)
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Deregulated MAP kinase (MAPK) signaling plays key roles in developmental and adult disease processes, but the experimental activation of MAPK is a currently unresolved task. For the reversible induction of MAPK signaling, we generated transgenic mice harboring a tamoxifen inducible BRAF(V637E) ER(T2) fusion protein. The expression of the inducible BRAF kinase can be directed by Cre/loxP-mediated recombination to selected cell types and enables the highly specific activation of MAPK signalling in vivo. We show that MAPK signaling can be transiently activated in the brain, liver, or kidney of Braf(V637E) ER(T2) mice by a single injection of tamoxifen. Braf(V637E) ER(T2) mice provide a new versatile tool to study disease mechanisms elicited by MAPK activation, complementing gene knockout technology that is restricted to the analysis of loss-of-function phenotypes. genesis 1-8.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Mapk ; Braf ; Tamoxifen ; Estrogen Receptor ; Rosa26 ; Cre ; Loxp ; Transgenic Mice; B-raf ; Recombinase Activity ; Cre ; Proteins ; Erk ; Disorders ; Mechanism ; Apoptosis ; Pathway ; Models
ISSN (print) / ISBN 1526-954X
e-ISSN 1526-968X
Quellenangaben Band: 51, Heft: 6, Seiten: 448-455 Artikelnummer: , Supplement: ,
Verlag Wiley
Begutachtungsstatus Peer reviewed