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APP Delta C31 (C-terminal)
AS21 4571 | Clonality: Polyclonal | Host: Rabbit | Reactivity: Human, mouse, rat
- Product Info
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Immunogen: KLH-conjugated synthetic peptide corresponding to the C-terminal of the caspase 3-cleaved human APP (aa 658-664 of human APP695) UniProt: P05067 Host: Rabbit Purity: Serum. Contains 0.05 % sodium azide. Format: Liquid Quantity: 100 µl Storage: Store at -20°C; make aliquots to avoid repeated freeze-thaw cycles. Please remember to spin the tubes briefly prior to opening them to avoid any losses that might occur from material adhering to the cap or sides of the tube. Tested applications: ELISA (ELISA), Immunolocalisation (IL), Western blot (WB) Recommended dilution: 1:500 - 1: 1000 (Immunocytochemistry), 1:1000 - 1: 3000 (WB) Expected | apparent MW: 86,9 | 96 kDa - Reactivity
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Confirmed reactivity: Human, mouse, rat Predicted reactivity: Species of your interest not listed? Contact us - Application Examples
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Human NT2 neurons (neurally differentiated human NT2 embryonic carcinoma cells) were infected with adenovirus vector expressing beta-galactosidase (1), wild-type APP (2) or APPdelta C31 (3). Cell lysates were prepared 48 h after infection, and proteins were analysed by Western blotting. Neurons overexpressing wild-type APP contained a 96 kD SAC-immunoreactive fragment which was also detected in APP delta C31-overexpressing neurons.
Neurally differentiated NT2 cells were cultured for 96 h in the absence of fetal calf serum. Cells were triply labeled for MAP2, the neuronal marker microtubule-associated protein 2 (MAP2), chromosomal DNA (Hoechst), and APP delta C31 (SAC). MAP2-immunopositive neurons with apoptotic nuclei (arrows) are intensively labelled with anti-APP delta C31 antibodies. The cells were fixed with 4 % formaldehyde and blocked with 4 % non-fat milk and 5 % goat normal serum at 4°C/ON.
- Background
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Background: The Alzheimer amyloid precursor protein (APP) is a transmembrane protein whose abnormal processing is associated with the pathogenesis of Alzheimer’s disease. APP695 lacking the protease inhibitor domain is the predominant form in neuronal tissues. APP695 is cleaved by caspases into the 664-residue amino (N)-terminal fragment that lacks the carboxyl C-terminal 31-residues (APP delataC31) and the 31-residues C-terminal fragment (APP-C31). APP delta C31 potentially plays pathophysiological roles in neuronal death. - Product Citations
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Selected references: Nishimura et al (2003). Upregulation and antiapoptotic role of endogenous Alzheimer amyloid precursor protein in dorsal root ganglion neurons. Exp Cell Res. 2003 Jun 10;286(2):241-51. doi: 10.1016/s0014-4827(03)00066-1. PMID: 12749853.
Nishimura et al. (2002) Cell death induced by a caspase-cleaved transmembrane fragment of the Alzheimer amyloid precursor protein. Cell Death Differ. 2002 Feb;9(2):199-208. doi: 10.1038/sj.cdd.4400931. PMID: 11840170. - Protocols
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