Amyloid Precursor Protein (APP, Amyloid beta (A4) Precursor Protein)

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1/Tip60 and inhibit Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity. Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. May be involved in copper homeostasis/oxidative stress through copper ion reduction. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. Rat and mouse beta-amyloid peptides bind only weakly transient metals and have little reducing activity due to substitutions of transient metal chelating residues. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation (By similarity). The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis. SUBUNIT: Binds, via its C-terminus, to the PID domain of several cytoplasmic proteins, including APBB family members, the APBA family, MAPK8IP1, SHC1, Numb and Dab1. Binding to Dab1 inhibits its serine phosphorylation. Also interacts with GPCR-like protein BPP, FPRL1, APPBP1, IB1, KNS2 (via its TPR domains), APPBP2 (via BaSS) and DDB1. In vitro, it binds MAPT via the MT-binding domains. Associates with microtubules in the presence of ATP and in a kinesin-dependent manner. Interacts, through a C-terminal domain, with GNAO1. Amyloid beta-42 binds CHRNA7 in hippocampal neurons. Beta-amyloid associates with HADH2. \n\nTissue Specificity:\ndifferent isoforms in different tissues: kidney. brain. liver. hippocampus, substania nigra pars compacta and cerebellum. In the cerebellum, all the isoforms are abundantly expressed in Purkinje cells.\n\nApplications: \nSuitable for use in Immunohistochemistry. Other applications not tested.\n\nRecommended Dilution:\nOptimal dilutions to be determined by the researcher.\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. For long-term storage and to avoid repeated freezing and thawing, aliquot Store at -20 degrees C. Aliquots are stable for at least 12 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

A2275-85C

Size

100ul

Applications

IHC

Hosts

Rabbit

Reactivities

Rat

Form

Supplied as a lyophilized powder. Reconstitute in 100ul of sterile water. Centrifuge to remove any insoluble material.

P Type

Pab

Purity

Serum

References

1. Wilson, C.A., et al., J. Neurosci. Res. 74: 361-369 (2003). ; 2. Andreasen, N., et al., World J. Biol. Psychiatry 4: 147-155 (2003). ; 3. Guenette, S.Y. Neuromolecular Med. 4: 147-160 (2003).

Additional Info

Specificity for APP was confirmed by IHC. Species Crossreactivity: This antiserum is known to react with rat APP. Reactivity with other species have not yet been tested.

Alternative Names

AAA, ABETA, ABPP, AD1, Alzheimer disease, Amyloid beta A4 protein precursor isoform b, Amyloid beta A4 protein precursor isoform c, Amyloid beta-peptide, APPI, Cerebral vascular amyloid peptide, CVAP, PN2