Structure of the Human N-Cadherin Gene: YAC Analysis and Fine Chromosomal Mapping to 18q11.2

Wallis, Julie; Fox, Margaret; Walsh, Frank S.

doi:10.1006/geno.1994.1358

Cited by 32 publications

(13 citation statements)

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“…In contrast to the conservation of the exon sizes, the introns varied widely in their sizes (22,(27)(28)(29)(30)(31). It has been suggested that the variation in the intron size prevents intergenic crossover events within the cadherin gene family (29).…”

Section: Discussionmentioning

confidence: 99%

Cloning of the Gene for Human Pemphigus Vulgaris Antigen (Desmoglein 3), a Desmosomal Cadherin

Silos

Tamai

et al. 1996

Journal of Biological Chemistry

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Pemphigus vulgaris antigen is a cadherin-like desmosomal cell adhesion molecule expressed primarily in suprabasal keratinocytes within the epidermis. Previously characterized structural features have defined this molecule as a desmoglein, DSG3. In this study, we have cloned the human DSG3 gene and examined the transcriptional regulation of its expression. The total gene consisted of 15 exons and was estimated to span >23 kilobases. Comparison of exon-intron organization of DSG3 with bovine DSG1 and several classical cadherin genes revealed striking conservation of the structure. Up to 2.8 kilobases of the upstream genomic sequences were sequenced and found to contain several putative cis-regulatory elements. The promoter region was GCrich and TATA-less, similar to previously characterized mammalian cadherin promoters. The putative promoter region was subcloned into a vector containing chloramphenicol acetyl transferase reporter gene. Transient transfections with a series of deletion clones indicated that the DSG3 promoter demonstrated keratinocytespecific expression, as compared with dermal fibroblasts examined in parallel, and fine mapping identified a 30-base pair segment at ؊200 to ؊170 capable of conferring epidermal specific expression. The results provide evidence for the transcriptional regulation of the pemphigus vulgaris antigen gene, potentially critical for development of the epidermis and physiologic terminal differentiation of keratinocytes.

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Section: Discussionmentioning

confidence: 99%

Cloning of the Gene for Human Pemphigus Vulgaris Antigen (Desmoglein 3), a Desmosomal Cadherin

Silos

Tamai

et al. 1996

Journal of Biological Chemistry

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“…The gene is composed of 16 exons, and homology was found not only between human and mouse, but also between N-cadherin and other cadherins (Wallis et al, 1994). The protein exists of five extracellular cadherin repeats (EC1 to EC5), a transmembrane and a cytoplasmic part that are encoded by exons 4 to 13, 13 and 14, and 14 to 16, respectively.…”

Section: N-cadherinmentioning

confidence: 99%

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Derycke

Bracke²

2004

Int. J. Dev. Biol.

356

284

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Cell migration is a process which is essential during embryonic development, throughout adult life and in some pathological conditions. Cadherins, and more specifically the neural cell adhesion molecule N-cadherin, play an important role in migration. In embryogenesis, N-cadherin is the key molecule during gastrulation and neural crest development. N-cadherin mediated contacts activate several pathways like Rho GTPases and function in tyrosine kinase signalling (for example via the fibroblast growth factor receptor). In cancer, cadherins control the balance between suppression and promotion of invasion. E-cadherin functions as an invasion suppressor and is downregulated in most carcinomas, while N-cadherin, as an invasion promoter, is frequently upregulated. Expression of N-cadherin in epithelial cells induces changes in morphology to a fibroblastic phenotype, rendering the cells more motile and invasive. However in some cancers, like osteosarcoma, N-cadherin may behave as a tumour suppressor. N-cadherin can have multiple functions: promoting adhesion or induction of migration dependent on the cellular context. KEY WORDS: N-cadherin, cancer, embryogenesis, invasion, signallingInt. J. Dev. Biol. 48: 463-476 (2004) Migration and invasionCell migration is a process that is essential during embryonic development and throughout further life. In the adult, cell migration is crucial for homeostatic processes, such as effective immune responses and repair of injured tissues. To migrate, the individual cell body must modify its shape to interact with the surrounding tissue structures. The extracellular matrix (ECM) forms a substrate, as well as a barrier for the advancing cell body. Cell migration through tissues results from a continuous cycle of interdependent steps. In general, there are five steps involved in cell migration in the ECM. First comes the protrusion of the leading edge, where growing actin filaments connect to adapter proteins and push the cell membrane in an outward direction. In a second step cell-matrix interactions and focal contacts are formed. After that, surface proteases such as matrix metalloproteinases (MMP) are recruited and focal proteolysis takes place. Then the cell contracts by actomyosin activation, and finally the tail of the cell is detached from its substrate (Friedl and Wolf, 2003).Border cells of the Drosophila melanogaster ovary are nowadays used as a model for migration. There are three recently discovered signalling pathways that control distinct aspects of migration: a global steroid-hormone signal defines the timing of migration, a highly localised cytokine signal that activates the Janus kinase-signal transducer and activator of transcription is both necessary and sufficient to induce migration, and finally, a growth factor that is analogous to platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) contributes to guiding the cells to their destination (Montell, 2003).In embryonic morphogenesis two types of collective cell movement can ...

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“…Taking this in account, the minimum genomic size of the gene is 120 kb. The size of the Br-cadherin gene is comparable to other cadherin genes that might span genomic regions of 200 kb or more (23,24). Br-cadherin has an unusually long 5Ј-UTR encoded by five separate exons, with the ORF beginning in exon 5.…”

Section: Resultsmentioning

confidence: 98%

Molecular characterization of Br-cadherin, a developmentally regulated, brain-specific cadherin

Selig

Lidov²,

Bruno³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Cadherins are a family of transmembrane proteins that play a crucial role in cell adhesion and in morphogenesis. Several of the cadherins are expressed in the nervous system, but none is neuron-specific. We characterize a new member of the cadherin family, Br-cadherin, which is present exclusively in the central nervous system. Although the Br-cadherin protein is confined to the central nervous system, its mRNA is present in several additional tissues, suggesting that there is posttranscriptional control of this gene's expression. Within the central nervous system, Brcadherin appears to be expressed specifically by neurons. In the mouse, its expression becomes detectable during the first postnatal week, which corresponds temporally to the onset of synaptogenesis and dendrite outgrowth in the brain. This pattern of expression is consistent with a role for Br-cadherin in neuronal development, perhaps specifically with synaptogenesis.

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Structure of the Human N-Cadherin Gene: YAC Analysis and Fine Chromosomal Mapping to 18q11.2

Cited by 32 publications

References 0 publications

Cloning of the Gene for Human Pemphigus Vulgaris Antigen (Desmoglein 3), a Desmosomal Cadherin

Cloning of the Gene for Human Pemphigus Vulgaris Antigen (Desmoglein 3), a Desmosomal Cadherin

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Molecular characterization of Br-cadherin, a developmentally regulated, brain-specific cadherin

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