|Calculated MW||99809 Da|
|Positive Control||Western blot:Huvec, C6 and Hela cell lysates.|
|Application & Usage||WB: 1:1000 – 1:10000.|
|Other Names||CDH2, CDHN, NCAD, Cadherin-2, CDw325|
|Formulation||In 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||N-Cadherin Antibody (Clone # EPR1791-4) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; 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. CDH2 may be involved in neuronal recognition mechanism. In hippocampal neurons, may regulate dendritic spine density (By similarity).|
|Cellular Location||Cell membrane; Single-pass type I membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
Thy1 is a GPI-anchored, developmentally regulated protein involved in various signaling cascades that mediate neurite outgrowth, T cell activation, tumor suppression, apoptosis, and fibrosis. It is highly expressed on the surface of adult neurons and is thought to play a role in modulating adhesive and migratory events, such as neurite extension. Decreased Thy1 expression is associated with the development of epithelial ovarian cancer, revealing its role as a putative tumor suppressor gene of human ovarian cancer. Thy1 knockout mice have impaired cutaneous immune responses and abnormal retinal development. Thy1 is epigenetically regulated or deregulated in some disease states, such as pulmonary fibrosis. The potentially reversible hypermethylation of the Thy1 promoter offers the possibility of novel therapeutic options in this disease.
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