Anti-N-Cadherin / CDH2, clone 13A9

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced) and 0.05% sodium azide. Recognizes a protein of ~140 kDa, identified as N-Cadherin (NCAD), also known as CDH2 and CD325. NCAD is a member of the Cadherin superfamily, and consists of five extracellular repeats, a transmembrane domain and a cytoplasmic domain. NCAD/CD325 deficient mice die at day 10 of gestation and embryos display major heart defects and malformed neural tubes and somites. Consistent with this, the protein has been implicated in several aspects of cardiac development including the precardiac mesoderm, establishment of left-right symmetry and cardiac looping morphogenesis. Furthermore, it is normally involved in inducing cell cycle arrest and its expression is frequently deregulated in cancer cells. Studies have linked N-cadherin to cancer metastasis by showing the aggressive tumor cells had preferentially turned on N-cadherin as opposed to E- or P-cadherin. Protein function: Calcium-dependent cell adhesion protein, preferentially mediates homotypic cell-cell adhesion by dimerization with a CDH2 chain from another cell. Cadherins may thus contribute to the sorting of heterogeneous cell types. Acts as a regulator of neural stem cells quiescence by mediating anchorage of neural stem cells to ependymocytes in the adult subependymal zone: upon cleavage by MMP24, CDH2-mediated anchorage is affected, leading to modulate neural stem cell quiescence. Plays a role in cell-to-cell junction formation between pancreatic beta cells and neural crest stem (NCS) cells, promoting the formation of processes by NCS cells. CDH2 may be involved in neuronal recognition mechanism. In hippocampal neurons, may regulate dendritic spine density. [The UniProt Consortium]