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Birth defect gene identified

sure proper development. This suggests a potential therapy for embryos that are missing TGF-beta in the neural crest cells.

"This might be useful to try out some possible rescue experiments," Chai said.

Although Chai's current results apply only to mice, a paper last spring in Nature Genetics (Loeys et al., 2005) identified a handful of human families with inherited mutations in TGF-beta receptors and with a high incidence of craniofacial defects, including cleft palate and skull malformations.

If the signaling mechanism in mice were to carry over to humans, pharmaceutical researchers could start to investigate FGF as a potential supplement for pregnant women, analogous to folic acid for prevention of spina bifida.

Chai noted that the FGF supplements in mice restored normal cell growth only in the skull region.

"Using FGF signaling we can actually rescue the cell proliferation defect, but so far we have not been able to do the same thing in the palate," Chai said.

TGF-beta also appears to work through different mechanisms in other parts of the body, Chai added. This suggests that no single treatment can correct all birth defects related to TGF-beta.


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Contact: Carl Marziali
marziali@usc.edu
213-740-4751
University of Southern California
22-Dec-2005


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