APP Antibody

Black line: Control Antigen (100 ng);
Purple line: Antigen(10ng);
Blue line: Antigen (50 ng);
Red line: Antigen (100 ng);
Figure 1: Western blot analysis using APP mAb against human APP (AA: 483-699) recombinant protein. (Expected MW is 50.7 kDa)
Figure 2: Western blot analysis using APP mAb against HEK293 (1) and APP (AA: 483-699)-hIgGFc transfected HEK293 (2) cell lysate.
Figure 3: Flow cytometric analysis of Hela cells using APP mouse mAb (green) and negative control (red).

SPECIFICATION
CITATIONS
PROTOCOLS
BACKGROUND

Product Information
Application Applications Legend: WB=Western Blot IHC=Immunohistochemistry IHC-P=Immunohistochemistry (Paraffin-embedded Sections) IHC-F=Immunohistochemistry (Frozen Sections) IF=Immunofluorescence FC=Flow Cytopmetry IC=Immunochemistry ICC=Immunocytochemistry E=ELISA IP=Immunoprecipitation DB=Dot Blot CHIP=Chromatin Immunoprecipitation FA=Fluorescence Assay IEM=Immunoelectronmicroscopy EIA=Enzyme Immunoassay	WB, FC, E
Primary Accession	P05067
Reactivity	Human
Host	Mouse
Clonality	Monoclonal
Clone Names	5H10A10
Isotype	IgG2b
Calculated MW	87kDa
Description	This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene.
Immunogen	Purified recombinant fragment of human APP (AA: 483-699) expressed in E. Coli.
Formulation	Purified antibody in PBS with 0.05% sodium azide.

Additional Information
Gene ID	351
Other Names	Amyloid beta A4 protein, ABPP, APPI, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, CVAP, PreA4, Protease nexin-II, PN-II, N-APP, Soluble APP-alpha, S-APP-alpha, Soluble APP-beta, S-APP-beta, C99, Beta-amyloid protein 42, Beta-APP42, Beta-amyloid protein 40, Beta-APP40, C83, P3(42), P3(40), C80, Gamma-secretase C-terminal fragment 59, Amyloid intracellular domain 59, AICD-59, AID(59), Gamma-CTF(59), Gamma-secretase C-terminal fragment 57, Amyloid intracellular domain 57, AICD-57, AID(57), Gamma-CTF(57), Gamma-secretase C-terminal fragment 50, Amyloid intracellular domain 50, AICD-50, AID(50), Gamma-CTF(50), C31, APP, A4, AD1
Dilution	E~~1/10000 WB~~1/500 - 1/2000 FC~~1/200 - 1/400
Storage	Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
Precautions	APP Antibody is for research use only and not for use in diagnostic or therapeutic procedures.

Protein Information
Name	APP (HGNC:620)
Function	Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed:25122912). Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits 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 (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1 (By similarity). By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapses in axons (PubMed:17062754, PubMed:23011729). Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1. N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).
Cellular Location	Cell membrane; Single-pass type I membrane protein. Membrane; Single-pass type I membrane protein. Perikaryon Cell projection, growth cone. Membrane, clathrin-coated pit. Early endosome. Cytoplasmic vesicle. Note=Cell surface protein that rapidly becomes internalized via clathrin-coated pits. Only a minor proportion is present at the cell membrane; most of the protein is present in intracellular vesicles (PubMed:20580937) During maturation, the immature APP (N-glycosylated in the endoplasmic reticulum) moves to the Golgi complex where complete maturation occurs (O-glycosylated and sulfated). After alpha-secretase cleavage, soluble APP is released into the extracellular space and the C-terminal is internalized to endosomes and lysosomes. Some APP accumulates in secretory transport vesicles leaving the late Golgi compartment and returns to the cell surface. APP sorts to the basolateral surface in epithelial cells. During neuronal differentiation, the Thr-743 phosphorylated form is located mainly in growth cones, moderately in neurites and sparingly in the cell body (PubMed:10341243). Casein kinase phosphorylation can occur either at the cell surface or within a post-Golgi compartment. Associates with GPC1 in perinuclear compartments. Colocalizes with SORL1 in a vesicular pattern in cytoplasm and perinuclear regions. [C99]: Early endosome [Amyloid-beta protein 40]: Cell surface [Gamma-secretase C-terminal fragment 59]: Nucleus. Cytoplasm Note=Located to both the cytoplasm and nuclei of neurons. It can be translocated to the nucleus through association with APBB1 (Fe65) (PubMed:11544248). In dopaminergic neurons, the phosphorylated Thr-743 form is localized to the nucleus (By similarity) {ECO:0000250\|UniProtKB:P12023, ECO:0000269\|PubMed:11544248}
Tissue Location	Expressed in the brain and in cerebrospinal fluid (at protein level) (PubMed:2649245). Expressed in all fetal tissues examined with highest levels in brain, kidney, heart and spleen. Weak expression in liver. In adult brain, highest expression found in the frontal lobe of the cortex and in the anterior perisylvian cortex- opercular gyri. Moderate expression in the cerebellar cortex, the posterior perisylvian cortex-opercular gyri and the temporal associated cortex. Weak expression found in the striate, extra-striate and motor cortices. Expressed in cerebrospinal fluid, and plasma. Isoform APP695 is the predominant form in neuronal tissue, isoform APP751 and isoform APP770 are widely expressed in non-neuronal cells. Isoform APP751 is the most abundant form in T-lymphocytes. Appican is expressed in astrocytes.

Research Areas

Primary Antibodies

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Application Protocols

Provided below are standard protocols that you may find useful for product applications.

Western Blot Protocol

Blocking Peptides Protocol

Dot Blot Protocol

Immunohistochemistry Protocol

Immunofluorescence Protocol

Immunoprecipitation Protocol

Flow Cytomety Protocol

Cell Culture Protocol

Background

The protein encoded by this gene belongs to putative adhesion molecule of myelomonocytic-derived cells that mediates sialic-acid dependent binding to cells. Preferentially binds to alpha-2,6-linked sialic acid. The sialic acid recognition site may be masked by cis interactions with sialic acids on the same cell surface. In the immune response, may act as an inhibitory receptor upon ligand induced tyrosine phosphorylation by recruiting cytoplasmic phosphatase(s) via their SH2 domain(s) that block signal transduction through dephosphorylation of signaling molecules. Induces apoptosis in acute myeloid leukemia (in vitro) and CD33 plays potential key roles in the pathogenesis of Alzheimer's disease (AD)

References

1. Proc Natl Acad Sci U S A. 2013 Sep 3;110(36):14604-9.2. ACS Chem Neurosci. 2013 Mar 20;4(3):454-62.

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