Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Craniofacial abnormalities induced by ectopic expression of the homeobox gene Hox-1.1 in transgenic mice.

MPG-Autoren
/persons/resource/persons14806

Balling,  R.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

/persons/resource/persons15156

Gruss,  P.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

/persons/resource/persons15322

Kessel,  M.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)

2382623.pdf
(Verlagsversion), 5MB

Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Balling, R., Mutter, G., Gruss, P., & Kessel, M. (1989). Craniofacial abnormalities induced by ectopic expression of the homeobox gene Hox-1.1 in transgenic mice. Cell, 58(2), 337-347. doi:10.1016/0092-8674(89)90848-9.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002C-3E33-1
Zusammenfassung
Hox-1.1 is a murine homeobox-containing gene expressed in a time- and cell-specific manner during embryogenesis. We have generated transgenic mice that ectopically express Hox-1.1 from the chicken β-actin promoter. In these mice Hox-1.1 expression was changed to an almost ubiquitous pattern. Ectopic expression of Hox-1.1 leads to death of the transgenic animals shortly after birth and is associated with multiple craniofacial anomalies, such as cleft palate, open eyes at birth, and nonfused pinnae. This phenotype is similar to the effects seen after systemic administration of retinoic acid during gestation. This suggests that retinoic acid embryopathy and the specific developmental defects caused by ectopic expression of a potential developmental control gene share a common pathogenic mechanism.