Dog Cadherin-2/N-Cadherin ELISA Kit (DEIABL615)

Regulatory status: For research use only, not for use in diagnostic procedures.

Write a review

cell culture supernates, serum, heparin plasma, EDTA plasma
Species Reactivity
Intended Use
Sandwich High Sensitivity ELISA kit for Quantitative Detection of Dog Caninea Cadherin-2/N-Cadherin.
Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles(Shipped with wet ice.)
Detection Range


Have you cited DEIABL615 in a publication? Let us know and earn a reward for your research.

Customer Reviews

Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket


N-cadherin is Required for Cytodifferentiation during Zebrafish Odontogenesis


Authors: Verstraeten, B.; van Hengel, J.; Sanders, E.; Van Roy, F.; Huysseune, A.

N-cadherin is a well-studied classic cadherin involved in multiple developmental processes and is also known to have a signaling function. Using the zebrafish (Danio rerio) as a model, we tested the hypothesis that tooth morphogenesis is accompanied by dynamic changes in N-cadherin distribution and that absence of N-cadherin disturbs tooth development. N-cadherin, encoded by the gene cdh2, is absent during the initiation and morphogenesis stages of both primary (first-generation) and replacement teeth, as demonstrated by immunohistochemistry. However, N-cadherin is up-regulated at the onset of differentiation of cells of the inner dental epithelium and the dental papilla, i.e., the ameloblasts and odontoblasts, respectively. In the inner dental epithelium, N-cadherin is co-expressed with E-cadherin, excluding the occurrence of cadherin switching such as observed during human tooth development. While early lethality of N-cadherin knockout mice prevents any functional study of N-cadherin in mouse odontogenesis, zebrafish parachute (pac) mutants, deficient for N-cadherin, survive beyond the age when primary teeth normally start to form. In these mutants, the first tooth forms, but its development stops at the early cytodifferentiation stage. N-cadherin deficiency also completely inhibits the development of the other first-generation teeth, possibly due to the absence of N-cadherin signaling once the first tooth has differentiated.

Disruption of CDH2/N-Cadherin-Based Adherens Junctions Leads to Apoptosis of Ependymal Cells and Denudation of Brain Ventricular Walls


Authors: Oliver, Cristian; Gonzalez, Cesar A.; Alvial, Genaro; Flores, Carlos A.; Rodriguez, Esteban M.; Federico Batiz, Luis

Disruption/denudation of the ependymal lining has been associated with the pathogenesis of various human CNS disorders, including hydrocephalus, spina bifida aperta, and periventricular heterotopia. It has been traditionally considered that ependymal denudation is a consequence of mechanical forces such as ventricular enlargement. New evidence indicates that ependymal disruption can precede ventricular dilation, but the cellular and molecular mechanisms involved in the onset of ependymal denudation are unknown. Here, we present a novel model to study ependymal cell pathophysiology and demonstrate that selective disruption of N-cadherin-based adherens junctions is sufficient to provoke progressive ependymal denudation. Blocking N-cadherin function using specific peptides that interfere with the histidine-alanine-valine extracellular homophilic interaction domain caused early pathologic changes characterized by disruption of zonula adherens and abnormal intracellular accumulation of N-cadherin. These changes then triggered massive apoptosis of ependymal cells and denudation of brain ventricular walls. Because no typical extrinsic mechanical factors such as elevated pressure or stretching forces are involved in this model, the critical role of N-cadherin-based adherens junctions in ependymal survival/physiology is highlighted. Furthermore, the results suggest that abnormal adherens junctions between ependymal cells should be considered as key components of the pathogenesis of CNS disorders associated with ependymal denudation.

Online Inquiry

Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:
Verification code
Click image to refresh the verification code.

Online Inquiry

  Interested in larger quantities ? request a quote!
  Protocol may be improved. Please feel free to contact us to obtain the latest version.!

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

OUR PROMISE TO YOU Guaranteed product quality expert customer support

Inquiry Basket