Overexpression of Smad2 in Tgf-β3-null mutant mice rescues cleft palate

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Modulation of lipid metabolic defects rescues cleft palate in Tgfbr2 mutant mice.

Mutations in transforming growth factor beta (TGFβ) receptor type II (TGFBR2) cause Loeys-Dietz syndrome, characterized by craniofacial and cardiovascular abnormalities. Mice with a deletion of Tgfbr2 in cranial neural crest cells (Tgfbr2(fl/fl);Wnt1-Cre mice) develop cleft palate as the result of abnormal TGFβ signaling activation. However, little is known about metabolic processes downstream ...

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Cleft palate represents one of the most common congenital birth defects in human. During embryonic development, palatal shelves display oronasal (O-N) and anteroposterior polarity before the onset of fusion, but how the O-N pattern is established and how it relates to the expansion and fusion of the palatal shelves are unknown. Here we address these questions and show that O-N patterning is ass...

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ژورنال

عنوان ژورنال: Developmental Biology

سال: 2005

ISSN: 0012-1606

DOI: 10.1016/j.ydbio.2004.10.023