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.
Page: 1 2 Related biology news :1
Contact: Carl Marziali
University of Southern California
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