Molecular consequences of a frameshifted DLX3 mutant leading to Tricho-Dento-Osseous syndrome.
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Tricho-dento-osseous syndrome: diagnosis and dental managementNeural crest deletion of Dlx3 leads to major dentin defects through down-regulation of Dsppp63 in skin development and ectodermal dysplasias.Mutant DLX 3 disrupts odontoblast polarization and dentin formation.Immortalized mouse floxed Bmp2 dental papilla mesenchymal cell lines preserve odontoblastic phenotype and respond to BMP2.Development and characterization of a mouse floxed Bmp2 osteoblast cell line that retains osteoblast genotype and phenotype.Transcriptional factor DLX3 promotes the gene expression of enamel matrix proteins during amelogenesis.SUMOylation of DLX3 by SUMO1 promotes its transcriptional activity.Bmp2 deletion causes an amelogenesis imperfecta phenotype via regulating enamel gene expressionMicroRNA 665 Regulates Dentinogenesis through MicroRNA-Mediated Silencing and Epigenetic MechanismsThe transcription factor DLX3 regulates the osteogenic differentiation of human dental follicle precursor cells.In vivo impact of a 4 bp deletion mutation in the DLX3 gene on bone development.The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growthImmortalized mouse dental papilla mesenchymal cells preserve odontoblastic phenotype and respond to bone morphogenetic protein 2.S100A14, a member of the EF-hand calcium-binding proteins, is overexpressed in breast cancer and acts as a modulator of HER2 signaling.A novel DLX3-PKC integrated signaling network drives keratinocyte differentiation.Amelogenesis Imperfecta; Genes, Proteins, and Pathways.A dominant mutation etiologic for human tricho-dento-osseous syndrome impairs the ability of DLX3 to downregulate ΔNp63α.Osteogenesis Imperfecta Type I Caused by COL1A1 Deletions.BMP-2 induced Dspp transcription is mediated by Dlx3/Osx signaling pathway in odontoblasts.Genetic variants in pachyonychia congenita-associated keratins increase susceptibility to tooth decay.Homeobox transcription factor DLX4 is not necessary for skin development and homeostasis.DLX3-dependent STAT3 signaling in keratinocytes regulates skin immune homeostasis.DLX3-Dependent Regulation of Ion Transporters and Carbonic Anhydrases is Crucial for Enamel Mineralization.Anthropoid primate-specific retroviral element THE1B controls expression of CRH in placenta and alters gestation length
P2860
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P2860
Molecular consequences of a frameshifted DLX3 mutant leading to Tricho-Dento-Osseous syndrome.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@ast
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@en
type
label
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@ast
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@en
prefLabel
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@ast
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@en
P2093
P2860
P356
P1476
Molecular consequences of a fr ...... Tricho-Dento-Osseous syndrome.
@en
P2093
Frederic Jaisser
Jane B Lian
Maria I Morasso
Mohammad Q Hassan
Olivier Duverger
Susie X Chen
P2860
P304
20198-20208
P356
10.1074/JBC.M709562200
P407
P577
2008-05-19T00:00:00Z