A TWIST in development

Rose, Charlotte; Malcolm, Sue

doi:10.1016/s0168-9525(97)01296-1

Cited by 42 publications

(30 citation statements)

References 31 publications

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“…24 Consequently, the presence of missense mutations at equivalent residues in the DNA-binding domain of TWIST (in 2/40 patients) suggests a dominant negative effect in these two cases. 25 However, the recent On the other hand, it is worth noting that 4/22 ACS III patients failed to harbour TWIST mutations in our series. One can speculate that these patients carry short scale deletions flanking the TWIST gene and downregulating its expression via a positional effect, especially as a translocation deletion located 5 kb downstream from the TWIST gene has been recently described in association with mild ACS III.…”

Section: Discussionmentioning

confidence: 54%

Mutations within or upstream of the basic helix–loop–helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome

Ghouzzi¹,

Lajeunie²,

Merrer³

et al. 1999

Eur J Hum Genet

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Section: Discussionmentioning

confidence: 54%

Mutations within or upstream of the basic helix–loop–helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome

Ghouzzi¹,

Lajeunie²,

Merrer³

et al. 1999

Eur J Hum Genet

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“…TWIST was originally identified in Drosophila for its role in gastrulation, mesoderm formation, and myogenesis (57). The human TWIST gene encodes a 21-kd protein that shares extensive homology with the mouse and Drosophila Twist proteins (58).…”

Section: Discussionmentioning

confidence: 99%

“…Basic HLH transcription factors such as Twist form either hetero-or homodimers in order to bind a DNA consensus sequence, called an E-box, that is found in the promoters of numerous genes. These factors can either inhibit or activate the transcription of other genes through binding to E-box sites, or by other mechanisms such as transcription factor sequestration (57,59).…”

Section: Discussionmentioning

confidence: 99%

“…It has been hypothesized that TWIST might regulate chondrogenesis by promoting or maintaining the prechondrogenic cell phenotype, and that differentiation into chondrocytes proceeds through downregulation of TWIST expression (57,60). Indeed, TWIST expression in the developing mouse coincides with areas adjacent to chondrogenic differentiation, such as those surrounding cells expressing the embryonic type IIA procollagen variant (60).…”

Section: Discussionmentioning

confidence: 99%

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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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“…The first exon contains an open reading frame encoding a 202 amino acid protein (GenPept: AAC50930.1) being, currently, only one transcript characterized (GenBank: NM_000474 and Ensembl: ENST00000242261). In human, the TWIST1 gene maps to 7p21.1 and is expressed in the head and limb buds in *Address correspondence to this author at the Institute for Biotechnology and Bioengineering, Centre of Genetics and Biotechnology, (IBB, CGB-UTAD), University of Trás-os-Montes and Alto Douro, Quinta de Prados, 5001-801 Vila Real, Portugal; Tel: +351259350841; Fax: +351259350572; E-mail: rchaves@utad.pt developing embryos [4]. In adult human, its expression is predominantly detected in mesodermally derived tissues [5].…”

Section: Introductionmentioning

confidence: 99%

TWIST1 Gene: First Insights in Felis Catus

2014

Advances in Genome Science

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TWIST1 is thought to be a novel oncogene. Understanding the molecular mechanisms regulating the TWIST1 gene expression profiles in tumor cells may give new insights regarding prognostic factors and novel therapeutic targets in veterinary oncology. In the present study we partially isolated the TWIST1 gene in Felis catus and performed comparative studies. Several primer combinations were used based on the alignments of homologous DNA sequences. After PCR amplification, three bands were obtained, purified and sequenced. Several bioinformatic tools were utilized to carry out the comparative studies. Higher similarity was found between the isolated TWIST1 gene in Felis catus and Homo sapiens (86%) than between Homo sapiens and Rattus norvegicus or Mus musculus (75%). Partial amino acid sequence showed no change in the four species analyzed. This confirmed that coding sequences presented high similarity (~96%) between man and cat. These results give the first insights regarding the TWIST1 gene in cat but further studies are required in order to establish, or not, its role in tumor formation and progression in veterinary oncology.

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A TWIST in development

Cited by 42 publications

References 31 publications

Mutations within or upstream of the basic helix–loop–helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome

Mutations within or upstream of the basic helix–loop–helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome

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

TWIST1 Gene: First Insights in Felis Catus

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