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£]igh3(TGF£]Ÿìinduced geneŸìh3), is an extracellular matrix protein,which
regulates cell proliferation, differentiation, wound healing,cellŸìcell
adhesion and apoptosis. The expression of £]igh3 is regulated by TGF£]3, a
critical signaling protein regulates embryonic palate development. Recently,
£]igh3 was reported to regulate apoptosis during embryonic palate fusion,
infer that TGF£]3 may regulate embryonic palate fusion through upregulating £]
igh3. Interferon regulatory factor 6 (IRF6) is a transcriptional factor which
also involves in embryonic palate fusion. Mutations in IRF6 cause Van der
Woude syndrome and popliteal pterygium syndrome, both of which show defects
in embryo palate fusion and epidermis fusion. However, the biological
function of IRF6 is still not clear. According to the predicted protein
functional domain, IRF6 may interact with Smad, an important signaling
protein in TGF£]3 pathway, suggesting that £]igh3, IRF6 and TGF£]3 may
cooperate to regulate palate development. To investigate the crosstalk within
£]igh3, IRF6 and TGF£]3 and the mechanisms that they regulate palate
development, we focus on searching the downstream genes of IRF6 in this
study. We first searched the downstream target genes of IRF6 with predicted
IRF6 binding consensus sequences by bioinformatics methods, and derived 12
candidate genes. Then we analyzed the expression changes of these target
genes after knockdown or overŸìexpression of IRF6 gene in epithelial cells.
Our results indicated that mRNA of NAPEPLD, PSRC1, DYRK1A, KIAA1841, CLDN23,
BUB1, IFIT5 and NBR1, as well as the BUB1 protein were upŸìregulated by IRF6
overexpression in HEK293T cell line. While the mRNA of KIAA1841, CLDN23, BUB1
and NBR1 were downŸìregulated when IRF6 expression was knockdown in CE48T/VGH
cells. These data suggesting that KIAA1841, CLDN23,BUB1 and NBR1 maybe the
downstream target genes of IRF6,however,the roles of these genes in embryonic
palate fusion still need further investigation.



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