Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-1-14
pubmed:abstractText
Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has been shown to be directly regulated by TGF-beta3. No phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was correlated with the persistence of the MEE and failure of palatal fusion. In the present study, the cleft palate phenotype in Tgf-beta3-/- mice was rescued by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-Smad2). Success of the rescue could be attributed to the elevated phospho-SMAD2 level in the MEE, demonstrated by two indirect evidences. The rescued palatal fusion in Tgf-beta3-/-/K14-Smad2 mice, however, never proceeded to the junction of primary and secondary palates and the most posterior border of the soft palate, despite phospho-SMAD2 expression in these regions at the same level as in the middle portion of the secondary palate. The K14-Smad2 transgene was unable to restore all the functional outcomes of TGF-beta3. This may indicate an anterior-posterior patterning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palatal fusion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0012-1606
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
193-202
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15649471-Animals, pubmed-meshheading:15649471-Animals, Newborn, pubmed-meshheading:15649471-Body Patterning, pubmed-meshheading:15649471-Cleft Palate, pubmed-meshheading:15649471-DNA-Binding Proteins, pubmed-meshheading:15649471-Gene Expression Regulation, Developmental, pubmed-meshheading:15649471-Mice, pubmed-meshheading:15649471-Mice, Inbred C57BL, pubmed-meshheading:15649471-Mice, Knockout, pubmed-meshheading:15649471-Mice, Transgenic, pubmed-meshheading:15649471-Palate, pubmed-meshheading:15649471-Phenotype, pubmed-meshheading:15649471-Phosphorylation, pubmed-meshheading:15649471-Signal Transduction, pubmed-meshheading:15649471-Smad2 Protein, pubmed-meshheading:15649471-Trans-Activators, pubmed-meshheading:15649471-Transforming Growth Factor beta, pubmed-meshheading:15649471-Transforming Growth Factor beta3
pubmed:year
2005
pubmed:articleTitle
Overexpression of Smad2 in Tgf-beta3-null mutant mice rescues cleft palate.
pubmed:affiliation
Center for Craniofacial Molecular Biology, School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103, Los Angeles, CA 90033, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.