References of "Kessel, M"
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See detailThe role of homeobox genes in mammalian development
Kessel, M; Balling, Rudi UL; Gruss, P

in Developmental Endocrinology (1990)

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See detailDevelopment(s) in mouse genetics.
Balling, Rudi UL; Kessel, M.

in Biochemistry & Cell Biology (1990), 68(2), 404-7

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See detailVariations of cervical vertebrae after expression of a Hox-1.1 transgene in mice.
Kessel, M.; Balling, Rudi UL; Gruss, P.

in Cell (1990), 61(2), 301-8

To understand the function of murine homeobox genes, a genetic analysis is mandatory. We generated gain-of-function mutants by introducing genomic sequences of the Hox-1.1 gene under the control of a ... [more ▼]

To understand the function of murine homeobox genes, a genetic analysis is mandatory. We generated gain-of-function mutants by introducing genomic sequences of the Hox-1.1 gene under the control of a chicken beta-actin promoter into mice. Our previous data had shown that these transgenic mice are nonviable after birth and are born with craniofacial abnormalities. In a subsequent detailed analysis of severely affected animals, malformations of the basioccipital bone, the atlas, and the axis were observed. Manifestation of an additional vertebra, a proatlas, occurred at the craniocervical transition. The dominant interference of the Hox-1.1 transgene with developmental programs seems to occur around day 9 of gestation, the time of neural crest migration and somite differentiation. We discuss the resulting phenotype with respect to a developmental control function of Hox-1.1. [less ▲]

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See detailCraniofacial abnormalities induced by ectopic expression of the homeobox gene Hox-1.1 in transgenic mice.
Balling, Rudi UL; Mutter, G.; Gruss, P. et al

in Cell (1989), 58(2), 337-47

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 beta ... [more ▼]

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 beta-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. [less ▲]

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