Cadherin-19 (CDH19) gene is one of three related type II cadherin genes situated in a cluster on chromosome 18, and CDH19 is closely clustered on a chromosome with CDH7 and CDH20. CDH19 is a 772 amino acid single-pass type I membrane protein that contains five cadherin domains, a transmembrane region and a highly conserved cytoplasmic tail. Expressed in a variety of tissues (such as heart, adrenal, colon and other tissues), CDH19 functions as a calcium-dependent cell-cell adhesion glycoprotein that is thought to be involved in the sorting of heterogeneous cell types. Since disturbance of intracellular adhesion is a prerequisite for invasion and metastasis of tumor cells, cadherins are considered prime candidates for tumor suppressor genes. Loss of cadherins may be associated with cancer formation. Alternative splicing results in multiple transcript variants for this gene.
Cadherins are calcium-dependent intercellular glycoproteins containing five extracellular cadherin (EC) repeats of about 110 amino acid residues with typical conserved sequences. The extracellular cadherin domains bind calcium, which is necessary for correct protein folding and normal functioning. All cadherins contain a transmembrane domain and a cytoplasmic domain, except for two variants that are anchored to the plasma membrane through a glycophosphotidyl-inositol (GPI) tail. The cytoplasmic domains of the classical (type I) and atypical (type II) cadherins contain conserved domains to which various catenins can bind. Type II (atypical) cadherins are defined based on their lack of a His-Ala-Val (HAV) cell adhesion recognition sequence specific to type I cadherins. Recent evidence suggests that changes in cadherin expression or “cadherin switching” play a critical role during tumor progression.
Fig.1 Structure of the classic cadherin protein family in humans. (Basu, 2015)
Sox10, a member of the HMG-domain Sox family of transcription factors, is known to play important roles in cell migration during the early formation of the enteric nervous system (ENS). Recent studies have shown that CDH-19 plays an important role in ENS development defects. CDH19 is a direct target of Sox10 during early sacral neural crest cells (NCCs) migration towards the hindgut and forms cadherin-catenin complexes which interact with the cytoskeleton in migrating cells. Elucidation of this novel molecular pathway helps to provide insights into the pathogenesis of ENS developmental defects.
Expression of CDH19 is restricted to minimally infiltrative GSC, with no detectable protein in other GSC, Glioblastoma multiforme (GBM), or normal neural cell lines on immunoblotting. These findings suggest that CDH19 (a type II atypical cadherin specific to myelinating cells during development), could serve as a feasible marker for GSC identification, isolation and drug discovery.
CDH19 is of particular interest since a human gene profiling study of mesenchymal tumors indicated it was upregulated in Schwannomas and Neurofibromas. A study suggested cad-19 could potentially be used as a marker for these tumors (mesenchymal, or bone and soft tissue tumor) during the screening process.
In addition, research indicates that CDH19 is down-regulated in colorectal cancer.
The cadherins are a superfamily of adhesion molecules that function in cell recognition, tissue morphogenesis and tumor suppression. The function of CDH19 is not understood clearly. Creative Biolabs provides a full set of CDH19 assay portfolio service, including but not limited to cell proliferation assays, TUNEL assay for cell apoptosis, neurite outgrowth assay, wound healing and cell migration assays, in situ hybridization (ISH), immunohistochemistry and immunocytochemistry, immunofluorescence, western blot.
Equipped with excellent expert teams and rich experience, Creative Biolabs is professional to provide comprehensive customized tumor marker assay services (e.g., Cadherin-19 assay portfolio service). Our one-stop services can assist your projects to succeed within the shortest timeline. Please feel free to contact us for more information.
Reference
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