twist is required in head mesenchyme for cranial neural tube morphogenesis.

Chen, Zhou Feng; Behringer, Richard R.

doi:10.1101/gad.9.6.686

Cited by 565 publications

(507 citation statements)

References 40 publications

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“…20 TWIST1 upregulation, however, has mainly been correlated with aggressive phenotypes, metastasis formation and poor prognosis. 3 TWIST1 is required for cell migration during both development 21 and oncogenesis. 22 Thus, TWIST1 downregulation might help primary tumor cells to remain localized early in breast cancer progression.…”

Section: Resultsmentioning

confidence: 99%

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Vislovukh

Meng

et al. 2012

Oncogene

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TWIST1 is a highly conserved basic helix-loop-helix transcription factor that promotes epithelial --mesenchymal transition (EMT). Its misregulation has been observed in various types of tumors. Using the MCF-10A-series of cell lines that recapitulate the early stages of breast cancer formation and EMT, we found TWIST1 to be upregulated during EMT and downregulated early in carcinogenesis. The TWIST1 3 0 UTR contains putative regulatory elements, including miRNA target sites and two cytoplasmic polyadenylation elements (CPE). We found that miR-580, CPEB1, and CPEB2 act as negative regulators of TWIST1 expression in a sequence-specific and additive/cooperative manner.

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Section: Resultsmentioning

confidence: 99%

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Vislovukh

Meng

et al. 2012

Oncogene

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“…In support of this hypothesis, it has been shown that in chimeric Sox9 Ϫ/Ϫ mice, mesenchymal cells deficient for SOX9 could not differentiate into chondrocytes (50). Mesenchymal cells in Twist knockout mice also display abnormalities in differentiation and proliferation, and overexpression of Twist in osteoblast-like cells inhibits their differentiation (77,78). It is likely that the combined down-regulation of SOX9 and up-regulation of TWIST in dedifferentiated cells is prohibitive for redifferentiation.…”

Section: Discussionmentioning

confidence: 97%

Assessment of the gene expression profile of differentiated and dedifferentiated human fetal chondrocytes by microarray analysis

Stokes¹,

Liu²,

Coimbra³

et al. 2002

Arthritis & Rheumatism

152

106

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Objective. To study the changes in patterns of gene expression exhibited by human chondrocytes as they dedifferentiate into fibroblastic cells in culture in order to better understand the mechanisms that control this process and its relationship to the phenotypic changes that occur in chondrocytes during the development of osteoarthritis (OA).Methods. Human fetal epiphyseal chondrocytes (HFCs) were cultured either on poly-(2-hydroxyethyl methacrylate)-coated plates (differentiated HFC cultures) or in plastic tissue culture flasks as monolayers (dedifferentiated HFC cultures). Following 11 days of culture under either condition, poly(A؉) RNA was isolated from the two cell populations and subjected to a gene expression analysis using a microarray containing ϳ5,000 known human genes and ϳ3,000 expressed sequence tags (ESTs).Results. A >2-fold difference in the expression of 62 known genes and 6 ESTs was observed between the two cell types. The differences in expression of several of the genes detected by the microarray hybridization were confirmed by Northern analyses. Two transcription factor genes, TWIST and HIF-1␣, and a cellular adhesion protein gene, cadherin 11, were markedly regulated in response to differentiation and dedifferentiation. Expression of these genes was also detected in adult normal and OA cartilage and chondrocytes. Analysis of the gene expression profile of HFCs revealed a complex pattern of gene expression, including many genes not yet reported to be expressed by chondrocytes.Conclusion. Chondrocytes in monolayer become dedifferentiated, acquiring a fibroblast-like appearance and changing their pattern of gene expression from one of expression of chondrocyte-specific genes to one that resembles a fibroblastic or chondroprogenitor-like pattern. Changes in gene expression associated with the process of dedifferentiation of HFCs in vitro were observed in a wide variety of genes, including genes encoding extracellular matrix proteins, transcription factors, and growth factors. At least 3 of the genes that were regulated in response to dedifferentiation were also found to be expressed in adult normal and OA articular cartilage and chondrocytes.

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“…Both reduced and increased numbers of head (Chen and Behringer, 1995;Zhao et al, 1996). Twist is expressed in head mesenchyme cells, and Twist knockout mice exhibit exencephaly (Chen and Behringer, 1995;Soo et al, 2002).…”

Section: Neural Patterning In Gcn5 Flox(neo)/⌬ Mutantsmentioning

confidence: 99%

“…Whole mount RNA in situ hybridization was performed as described (Nagy et al, 2003). The Twist, Ptc1, and Gli1 probes were kindly provided by Dr. R. Behringer (Chen and Behringer, 1995;Soo et al, 2002). Probes for Cart1 and Sox9 were kindly provided by Dr. B. de Crombrugghe (Dept.…”

Section: In Situ Hybridizationsmentioning

confidence: 99%

Proper expression of the Gcn5 histone acetyltransferase is required for neural tube closure in mouse embryos

Lin

Zhang

Srajer

et al. 2008

Developmental Dynamics

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Histone acetyltransferases (HATs) are important to gene activation, altering chromatin structures to facilitate association of transcription proteins with gene promoters. The functions of individual HATs in mammalian developmental are not well defined. Our previous studies demonstrated that Gcn5, a prototypical HAT, is required for mesodermal maintenance in early embryos. Homozygous Gcn5 null embryos die soon after gastrulation, preventing determination of Gcn5 functions later during development. We report here the creation of a Gcn5 flox(neo) allele, which is only partially functional and gives rise to a hypomorphic phenotype. Mice homozygous for this allele had an increased risk of cranial neural tube closure defects (NTDs) and exencephaly. These defects were found at an even greater penetrance in

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twist is required in head mesenchyme for cranial neural tube morphogenesis.

Cited by 565 publications

References 40 publications

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Assessment of the gene expression profile of differentiated and dedifferentiated human fetal chondrocytes by microarray analysis

Proper expression of the Gcn5 histone acetyltransferase is required for neural tube closure in mouse embryos

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