|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Recombinant Human Nicastrin / NCSTN protein (Catalog#11183-H08H)|
|10 μl/Test, 0.1 mg/ml|
|Aqueous solution containing 0.5% BSA and 0.09% sodium azide|
|This antibody was obtained from a rabbit immunized with purified, recombinant Human Nicastrin / NCSTN (rh Nicastrin / NCSTN; Catalog#11183-H08H; NP_056146.1; Met1-Glu669) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.|
|Human Nicastrin / NCSTN|
|This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !|
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Nicastrin (NCST, or NCT), a single-pass membrane glycoprotein that harbors a large extracellular domain, is an essential component of the gamma-secretase complex. Several lines of evidence indicate that the members of these complexes could also contribute to the control of cell death. NCT controls cell death via phosphoinositide 3-kinase/Akt and p53-dependent pathways and that this function remains independent of the activity and molecular integrity of the gamma-secretase complexes. Increasing evidences have shown that Nicastrin/NCSTN plays a crucial role in gamma-cleavage of the amyloid precursor protein (APP). The glycoprotein Nicastrin is an essential component of the gamma-secretase complex, a high molecular weight complex which also contains the presenilin proteins, Aph-1 and Pen-2. The gamma-secretase complex is not only involved in APP processing but also in the processing of an increasing number of other type I integral membrane proteins. As the largest subunit of the gamma-secretase complex, Nicastrin plays a crucial role in its activation. Inhibition of NCSTN demonstrated an altered gamma-cleavage activity, suggesting its potential implication in developing Alzheimer's disease (AD). In addition, Nicastrin can function to maintain epithelial to mesenchymal transition during breast cancer progression. Anti-nicastrin polyclonal and monoclonal antibodies were able to decrease notch1 and vimentin expression and reduced the invasive capacity of breast cancer cells in vitro.