Human N-Cadherin Alexa Fluor® 405-conjugated Antibody
Human N-Cadherin Alexa Fluor® 405-conjugated Antibody Summary
Asp160-Ala724
Accession # P19022.4
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
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Preparation and Storage
Background: N-Cadherin
Neuronal Cadherin (N-Cadherin or NCAD), also known as Cadherin-2 (CDH2), is a 130 kDa type I membrane protein belonging to the Cadherin superfamily of calcium-dependent adhesion molecules. Cadherins are involved in multiple processes including embryonic development, cell migration, and maintenance of epithelial integrity (1, 2). Human N‑Cadherin is synthesized with a 25 amino acid (aa) signal peptide and a 134 aa N‑terminal propeptide. The mature cell surface‑expressed protein consists of a 565 amino acid (aa) extracellular domain (ECD) that contains five Cadherin repeats, a 21 aa transmembrane segment, and a 161 aa cytoplasmic domain (3). Within the ECD, human N-Cadherin shares 98% aa sequence identity with mouse and rat N-Cadherin. In the nervous system, N-Cadherin mediates adhesion between the opposing faces of developing neuronal synapses and between Schwann cells and neuronal axons (4, 5). It interacts in cis or in trans homophilically and with the GluR2 subunit of neuronal AMPA receptors (1, 6). During synaptic maturation, its expression is lost from inhibitory terminals but maintained at excitatory terminals (5). ADAM10-mediated shedding of the N-Cadherin ECD alters cell-cell adhesion, synaptic development, and AMPA receptor activity (7, 8). N-Cadherin can also be cleaved at multiple additional sites within the intracellular or extracellular domains by Calpain, gamma ‑Secretase, and several MMPs (9-13). Cleavage of N‑Cadherin in atherosclerotic plaques contributes alternatively to vascular smooth muscle cell proliferation (MMP-9 and -12) or apoptosis (MMP‑7 (12, 13). Aberrant cell surface expression of the pro and mature forms of N-Cadherin in cancer results in increased tumor progression and invasiveness (14, 15). N‑Cadherin also mediates the adhesion between hematopoeitic progenitor cells and mesenchymal stromal cells of the bone marrow (16).
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