Erratum to “TWIST inactivation reduces CBFA1/RUNX2 expression and DNA binding to the osteocalcin promoter in osteoblasts” [Biochem. Biophys. Res. Commun. 297 (2002) 641–644]

Yousfi, Malika; Lasmoles, F.; Kern, Brigitt; Marie, Pierre J.

doi:10.1016/s0006-291x(03)00642-9

Cited by 3 publications

(2 citation statements)

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“…Twist is expressed by osteoprogenitors and as they differentiate they lose this expression [236]. TWIST inhibits bone formation by forming a transcriptional complex with, and negatively regulating, RUNX2 [272][273][274]. Loss-of-function mutations in TWIST in patients with Saethre-Chotzen syndrome can result in protein instability, an abolition of DNA binding or an inability of TWIST proteins to recruit dimer partners [275,276].…”

Section: Craniosynostosismentioning

confidence: 99%

“…As might be predicted loss-offunction mutations in TWIST do not cause CCD but result in craniosynostosis, a condition with excessive osteogenesis of the calvarial bones [136,137,271]. Twist is expressed by early osteoprogenitors but not by mature osteoblasts and has been suggested to act as a negative regulator of osteogenesis [236,273]. Double heterozygotes for Twist1 and Runx2 deletion show a partial rescue of the widened calvarial sutures seen in Runx2 +/-mice [274].…”

Section: Cleidocranial Dysplasiamentioning

confidence: 99%

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Craniofacial Anomalies: From Development to Molecular Pathogenesis

Rice¹

2005

CMM

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Advances in developmental biology combined with progress in human genetics are helping us decipher how the craniofacial region develops and how the consequences of misdirected development result in malformation. This review describes the molecular etiology of a number of craniofacial developmental anomalies. The more common craniofacial anomalies cleft lip and palate and craniosynostosis, as well as cleidocranial dysplasia, hemifacial microsomia, holoprosencephaly, enlarged parietal foramina, Treacher Collins syndrome and cherubism are discussed.

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Section: Craniosynostosismentioning

confidence: 99%

Section: Cleidocranial Dysplasiamentioning

confidence: 99%

Craniofacial Anomalies: From Development to Molecular Pathogenesis

Rice¹

2005

CMM

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Molecular silencing of Twist1 enhances osteogenic differentiation of murine mesenchymal stem cells: Implication of FGFR2 signaling

Miraoui

Sévère

Vaudin

et al. 2010

J of Cellular Biochemistry

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The capacity of mesenchymal stem cells (MSCs) to differentiate into functional osteoblasts is tightly controlled by transcription factors that trigger osteoblast commitment and differentiation. The role of Twist1, a basic helix-loop-helix (bHLH) transcription factor, in osteogenic differentiation of MSCs remains unclear. Here we investigated the role of Twist1 in the osteogenic differentiation program of murine C3H10T1/2 mesenchymal cells. We showed that molecular silencing of Twist1 using short hairpin RNA (shRNA) expression moderately increased C3H10T1/2 cell proliferation and had no effect on cell survival. In contrast, Twist1 silencing enhanced osteoblast gene expression and matrix mineralization in vitro. Biochemical analyses revealed that Twist1 silencing increased the expression of FGFR2 protein level, which was reduced by a mutant Runx2. Consistent with this finding, Twist1 silencing increased ERK1/2 and PI3K signaling. Moreover, molecular or pharmacological inhibition of FGFR2 or of ERK1/2 and PI3K signaling partly abolished the increased osteoblast gene expression induced by Twist1 silencing in C3H10T1/2 cells. These results reveal that Twist1 silencing upregulates osteoblast differentiation of murine mesenchymal cells in part via activation of FGFR2 expression and downstream signaling pathways, which provides novel insights into the molecular signals by which this transcription factor regulates the osteogenic differentiation program in MSCs.

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Estudo molecular das craniossinostoses sindrômicas: Crouzon, Pfeiffer e Saethre-Chotzen"

Oliveira¹

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Capítulo 1-Introdução geral e objetivos _____________________________ 04 1.1-Introdução Craniossinostoses___________________________________ 05 1.1.2-Craniossinostoses Sindrômicas _______________________________ 08 1.2-Aspectos clínicos das síndromes de craniossinostoses mais comuns _________________________________________________ 10 ABSTRACT Craniosynostosis, defined as the premature fusion of one or more cranial suture, are a very heterogeneous group of disorders, with an occurrence of about 1: 2000 live births. Except for rare syndromes, such as Apert, most of the cranioysnostotic conditions are characterized by wide clinical variability and genetic heterogeneity. Craniosynostosis can be classified into non syndromic forms-premature suture fusion is the only clinical alteration, and syndromic ones-premature cranial suture fusion associated with other anomalies. Apert, Pfeiffer, Crouzon and Saethre-Chotzen are the most common syndromic forms of craniosynostosis. The mutational mechanism is identified in approximately 58% of patients with Crouzon syndrome: FGFR2 mutations account for most of the cases (more than 80%) while mutations in TWIST1 and FGFR3 causes the remaining of them. Therefore, about 42% of the cases with clinical characteristics of Crouzon syndrome do not harbor mutations in any of these 3 genes and other mutational mechanisms might be responsible for the phenotype. Approximately 45% of Pfeiffer syndrome cases is not caused by mutations in the FGFR1 or FGFR2 genes, thus also suggesting genetic heterogeneity for this phenotype. On the other hand, all cases with Apert syndrome are caused by specific mutations in FGFR2. FGFR2 mutations show a partial genotype-phenotype correlation; however, severe cases, such as Pfeiffer types II and III are still very poorly characterized.

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Erratum to “TWIST inactivation reduces CBFA1/RUNX2 expression and DNA binding to the osteocalcin promoter in osteoblasts” [Biochem. Biophys. Res. Commun. 297 (2002) 641–644]

Cited by 3 publications

References 0 publications

Craniofacial Anomalies: From Development to Molecular Pathogenesis

Craniofacial Anomalies: From Development to Molecular Pathogenesis

Molecular silencing of Twist1 enhances osteogenic differentiation of murine mesenchymal stem cells: Implication of FGFR2 signaling

Estudo molecular das craniossinostoses sindrômicas: Crouzon, Pfeiffer e Saethre-Chotzen"

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