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T-614 promotes osteoblastic differentiation by increasing the expression of Osterix and Dlx5.
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Results indicate that Dlx5 and Runx2 are critical factors for the upregulated Osterix expression in shPP2A cells, which is considered to be important for the accelerated osteoblast differentiation in these cells.
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FGF10 pathway is downregulated in Dlx5(-/-) mice, and activation of FGF10 signaling rescues cranial neural crest cell proliferation and myogenic differentiation.
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High DLX5 expression is associated with T-cell lymphomagenesis.
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Both transient and stable expression of Necdin induced osteoblast-specific markers in an osteogenic cell line through formation of a complex with distal-less Homeobox 5 (Dlx5) and Runx2 promoter activation.
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DLX5 and DLX6 reciprocally inhibit BMP/H2-mediated H1 enhancer regulation in mandible embryonic development.
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We found that in Dlx5;6 DKO limbs, the AER expresses lower levels of Wnt5a, shows scattered beta-catenin responsive cells and altered basolateral and planar cell polarity (PCP).
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Dlx5 and Dlx6 expression determines uterine architecture and adenogenesis and is needed for implantation
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The results presented here indicate that loss of Dlx5 causes a down-modulation of miR-9 and of miR-200-class, which results in the over-expression of the Foxg1 protein.
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Lck-Dlx5 mice develop T-ALLs that consistently acquire overexpression of Myc and activation of Akt.
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Study demonstrated a novel role of miR-124 and Dlx5 in regulating the differentiation of mesenchymal stem cells toward the myogenic lineage, that is, miR-124 inhibits myogenic differentiation partially through targeting Dlx5 expression.
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Mash1 is required for the expression of GAD67 and Dlx5 in taste bud cells.
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Dlx5 and Mef2 directly bound to the runx2 enhancer, and the binding sites were required for the osteoblast-specific expression
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the prethalamic factors Dlxs upregulated by Ascl1/Helt deficiency play unique roles in regulating thalamic progenitor specification.
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Results show that DLX5, p63, Pin1 and FGF8 participate to the same time- and location-restricted regulatory loop essential for apical ectodermal ridge stratification, hence for normal patterning and skeletal morphogenesis of the limb buds.
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The Edn1/Ednra signaling regulates neural crest differentiation to ensure the proper patterning of pharyngeal arch arteries, which is independent of the mechanism mediated by Dlx5/Dlx6.
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Data show that Dlx5 and Msx2 play a critical role in controlling cranial neural tube morphogenesis by regulating cell adhesion via the ephrinA5 and EphA7 pathway.
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in AER cells and, at later stages, in the limb mesoderm the regulation of by Dlx5 and Dlx6 occurs also cell autonomously
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allelic reduction of Dlx5 and Dlx6 in the mouse results in a POI-like phenotype, characterized by reduced fertility and early follicular exhaustion.
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Dlx5, Msx2, and Runx2 enhancers exhibit a dual requirement for TCF/LEF1 and Smad binding element (SBE) sites that mediate synexpression of the three genes during osteoblast differentiation.
