Rabbit anti-Human Dact3 polyclonal antibody

Wnt signaling is essential for tooth formation and Dact proteins modulate Wnt signaling by binding to the intracellular protein Dishevelled (DvI). Comparison of the three known mouse Dact genes, Dact1-3, from the morphological initiation of mandibular first molar development through the onset of root formation using section in situ hybridization showed distinct, complementary and overlapping expression patterns for these genes. Whereas Dact2 expression was restricted to the dental epithelium, including the enamel knot signaling centers and pre-ameloblasts, Dact1 and Dact3 showed developmentally regulated expression in the dental mesenchyme. Both Dact1 and Dact3 mRNAs were first detected in the presumptive dental mesenchyme. After being downregulated from the condensing dental mesenchyme of the bud stage tooth germ, Dact1 was upregulated in the dental follicle mesenchyme at the cap stage and subsequently also in the dental papilla at the bell stage, where the expression persisted to the postnatal stages. In contrast, Dact3 transcripts persisted throughout the dental mesenchyme, including the preodontoblasts, during embryogenesis before transcripts were largely downregulated from the tooth germ postnatally. Collectively, these results suggest that Dact1 and -3 may contribute to early tooth formation by modulation of Wnt signaling pathways in the mesenchyme, including preodontoblasts, whereas Dact2 may play important signal-modulating roles in the adjacent epithelial cells including the enamel knot signaling centers and pre-ameloblasts. Future loss-of-function studies will help elucidate whether any of these functions are redundant, particularly for Dact1 and Dact3. (c) 2010 Elsevier B.V. All rights reserved.

Phthalates are endocrine-disrupting chemicals that can cross the placenta and affect the fetal epigenome. Among various epigenetic regulators of gene expression, long noncoding RNAs (lncRNAs) are important players that may also be involved in the manifestation of endocrine-disrupting chemical toxicity. We sought to explore the association between maternal urinary phthalate metabolite concentrations and lncRNA expression in human placenta to better understand potential mechanisms through which lncRNAs participate in mediating phthalate toxicity. Ten patients with uncomplicated dichorionic diamniotic twin pregnancies at term were included in this study. Urinary (n = 10) and placenta samples (n = 20) were collected for all participants. Urinary samples were analyzed for 15 phthalate metabolites and 2 phthalate alternative metabolites. Real-time PCR arrays were used to identify and quantify 87 lncRNAs from the placental samples. We tested the Spearman correlation matrix to compare prenatal phthalate measures against placental lncRNA levels. lncRNA levels showed large variations across samples, with no significant differences in lncRNA expression within twin pairs. Mono-(carboxynonyl) phthalate demonstrated consistently strong correlations with most lncRNAs. The strongest correlation was observed between mono-hydroxyisobutyl phthalate and LOC91450 (R-spearman = 0.88, p < .001). This correlation remained significant after Bonferroni adjustment. Other strong correlations were observed between mono-isobutyl phthalate, DPP10 and HOTTIP (R-spearman = -0.91, p < .001). AIRN, DACT3.AS1, DLX6, DPP10, HOTTIP, LOC143666, and LOC91450 were strongly correlated with the greatest number of phthalate metabolites. Further studies are needed to validate these results and understand if the altered expression of lncRNAs in human placenta has clinical significance.