Human CellExp E-Cadherin /ECAD /Cadherin-1/CD324 Protein, human recombinant protein
Cadherin-1, CDH1, CD324, E-cadherin, Arc-1, ECAD, LCAM, UVO
|Calculated MW||This protein is fused with 6×His tag at the C-terminus, has a calculated MW of 67 kDa. The predicted N-terminus is Gln 23. DTT-reduced Protein migrates as 67 kDa due to glycosylation.|
|Other Names||Cadherin-1, CDH1, CD324, E-cadherin, Arc-1, ECAD, LCAM, UVO|
|Application Notes||Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 µg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.|
|Storage||-20°C; Lyophilized from 0.22 µm filtered solution in PBS, pH7.4. Normally Mannitol or Trehalose is added as protectants before lyophilization.|
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Provided below are standard protocols that you may find useful for product applications.
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. Cadherin-1 (CDH1) also known as epithelial cadherin (E-cadherin), CD_antigen (CD324), Uvomorulin (UVO) ECAD and CDHE, CDH1 / CD324 contains 5 cadherin domains. CDH1 / CD324 / ECAD is expressed in non-neural epithelial tissues. CDH1 / E-CAD is involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells and has a potent invasive suppressor role. It is a ligand for integrin alpha-E/beta-7. E-Cad promotes non-amyloidogenic degradation of Abeta precursors and has a strong inhibitory effect on APP C99 and C83 production. Defects in CDH1 / CD324 / ECAD are the cause of hereditary diffuse gastric cancer (HDGC).
Bussemakers M.J.G.,et al.Mol. Biol. Rep. 17:123-128(1993).
Oda T.,et al.Proc. Natl. Acad. Sci. U.S.A. 91:1858-1862(1994).
Rimm D.L.,et al.Biochem. Biophys. Res. Commun. 200:1754-1761(1994).
Ito K.,et al.Oncogene 18:7080-7090(1999).
Shibamoto S.,et al.Submitted (MAR-1999) to the EMBL/GenBank/DDBJ databases.
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