Genetic interactions between Pax9 and Msx1 regulate lip development and several stages of tooth morphogenesis (Q28591953)

GOA release 2020-03-11

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Ralf Kist

6

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author name string

Mitsushiro Nakatomi

1

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31 January 2017

Xiu-Ping Wang

2

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31 January 2017

Darren Key

3

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31 January 2017

Jennifer J. Lund

4

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31 January 2017

Annick Turbe-Doan

5

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31 January 2017

Andrew Aw

7

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31 January 2017

Yiping Chen

8

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31 January 2017

Richard L. Maas

9

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31 January 2017

Heiko Peters

Runx2 mediates FGF signaling from epithelium to mesenchyme during tooth morphogenesis

10

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31 January 2017

language of work or name

English

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publication date

15 April 2010

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31 January 2017

Developmental Biology

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31 January 2017

340

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31 January 2017

2

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31 January 2017

438–449

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31 January 2017

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Progressive loss of PAX9 expression correlates with increasing malignancy of dysplastic and cancerous epithelium of the human oesophagus

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The LIM homeodomain transcription factors Lhx6 and Lhx7 are key regulators of mammalian dentition

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Shh signaling within the dental epithelium is necessary for cell proliferation, growth and polarization

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Localization of putative stem cells in dental epithelium and their association with Notch and FGF signaling.

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Reduction of Pax9 gene dosage in an allelic series of mouse mutants causes hypodontia and oligodontia.

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Expression of Notch 1, 2 and 3 is regulated by epithelial-mesenchymal interactions and retinoic acid in the developing mouse tooth and associated with determination of ameloblast cell fate

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MSX1 and orofacial clefting with and without tooth agenesis

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Characterization and developmental expression of Pax9, a paired-box-containing gene related to Pax1

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Lunatic fringe, FGF, and BMP regulate the Notch pathway during epithelial morphogenesis of teeth.

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Sonic hedgehog signaling is important in tooth root development

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Antagonistic interactions between FGF and BMP signaling pathways: a mechanism for positioning the sites of tooth formation

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Functional consequences of interactions between Pax9 and Msx1 genes in normal and abnormal tooth development.

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Pax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities.

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Mechanisms of ectodermal organogenesis

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Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development

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Genetic association studies of cleft lip and/or palate with hypodontia outside the cleft region

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Paradox segmentation along inter- and intrasomitic borderlines is followed by dysmorphology of the axial skeleton in the open brain (opb) mouse mutant.

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Mutation of PAX9 is associated with oligodontia

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Notch1 is essential for postimplantation development in mice.

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Homozygous mutations in fibroblast growth factor 3 are associated with a new form of syndromic deafness characterized by inner ear agenesis, microtia, and microdontia

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MSX1, PAX9, and TGFA contribute to tooth agenesis in humans.

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Follistatin regulates enamel patterning in mouse incisors by asymmetrically inhibiting BMP signaling and ameloblast differentiation

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Apc inhibition of Wnt signaling regulates supernumerary tooth formation during embryogenesis and throughout adulthood.

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Transgenically ectopic expression of Bmp4 to the Msx1 mutant dental mesenchyme restores downstream gene expression but represses Shh and Bmp2 in the enamel knot of wild type tooth germ.

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