Rabbit Monoclonal Amyloid-beta precursor protein antibody. Carrier free. Suitable for Dot, WB, I-ELISA and reacts with Synthetic peptide, Human samples.
pH: 7.2 - 7.4
Constituents: 100% PBS
IHC-P | Dot | WB | I-ELISA | |
---|---|---|---|---|
Human | Not recommended | Expected | Tested | Tested |
Synthetic peptide | Not recommended | Tested | Not recommended | Not recommended |
Species | Dilution info | Notes |
---|---|---|
Species Human, Synthetic peptide | Dilution info - | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Synthetic peptide | Dilution info 1/2000 | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 1/1000 | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Synthetic peptide | Dilution info - | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info - | Notes Use at 62.5ng/ml |
Species | Dilution info | Notes |
---|---|---|
Species Synthetic peptide | Dilution info - | Notes - |
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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. Amyloid-beta peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts. Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain. The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.
A4, AD1, APP, Amyloid-beta precursor protein, ABPP, APPI, Alzheimer disease amyloid A4 protein homolog, Alzheimer disease amyloid protein, Amyloid precursor protein, Amyloid-beta (A4) precursor protein, Amyloid-beta A4 protein, Cerebral vascular amyloid peptide, PreA4, Protease nexin-II, CVAP, PN-II
Rabbit Monoclonal Amyloid-beta precursor protein antibody. Carrier free. Suitable for Dot, WB, I-ELISA and reacts with Synthetic peptide, Human samples.
pH: 7.2 - 7.4
Constituents: 100% PBS
Human Eotaxin-2 Antibody Pair - BSA and Azide free ab244035 is a carrier free version of Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. The carrier-free buffer and high concentration allow for increased conjugation efficiency.
This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications.
Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Pyroglutamate beta amyloid also known by its abbreviation pGlu-Aβ is a modified form of beta amyloid that plays a significant role in the pathology of Alzheimer's disease. This peptide is approximately 40-42 amino acids in length contributing to its molecular mass range of 4 to 5 kDa. Pyroglutamate beta amyloid is generated through a post-translational modification where glutamate residues on beta amyloid undergo cyclization. This modification imparts stability and resistance to degradation causing it to accumulate in the brain. Researchers find pyroglutamate beta amyloid mainly in the neurons and plaques of the brains of Alzheimer’s patients.
Pyroglutamate beta amyloid affects neuronal function by increasing the aggregation propensity of beta amyloid. It enhances the toxic effects on synapses and neurons disrupting communication and leading to synaptic dysfunction. Pyroglutamate-modified amyloid beta is a component of the amyloid plaque complex which includes other amyloid peptides and metal ions. The presence of pGlu-Aβ in these plaques enhances their stability and neurotoxicity accelerating neuronal degradation and loss of cognitive functions.
Modified pyroglutamate beta amyloid involves itself in amyloidogenic pathways that include processes such as the beta-secretase and gamma-secretase pathways. These pathways lead to production and modification of amyloid beta peptide initiating plaque formation in the brain. The interaction of pyroglutamate beta amyloid with tau protein is significant as the aggregation of these proteins advances neurodegeneration. Tau proteins become hyperphosphorylated in response disrupting cellular transport and further promoting Alzheimer's disease progression.
Pyroglutamate beta amyloid connects closely with Alzheimer's disease where its modified form accelerates plaque formation and neurodegeneration. Researchers also study its role in frontotemporal dementia another neurodegenerative disorder characterized by tau protein dysfunction. The aggregation of pyroglutamate beta amyloid interacts with other forms of amyloid beta as well as tau contributing to the pathological hallmarks of these disorders.
We have tested this species and application combination and it works. It is covered by our product promise.
We have not tested this specific species and application combination in-house, but expect it will work. It is covered by our product promise.
This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
We do not recommend this combination. It is not covered by our product promise.
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This data was developed using Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034, the same antibody clone in a different buffer formulation.
Blocking and diluting buffer and concentration was 5% NFDM/TBST.
Lanes 1 - 2: Western blot - Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] (Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034) at 1/1000 dilution
Lanes 1 - 2: Western blot - Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] (ab290645) at 1/1000 dilution
Lane 1: beta Amyloid pE3-42 (aa674-713) peptide 100ng
Lane 2: beta Amyloid 1-42 (aa672-713) peptide 100ng
All lanes: Western blot - Goat Anti-Rabbit IgG H&L (HRP) (Goat Anti-Rabbit IgG H&L (HRP) ab97051) at 1/1000000 dilution
Exposure time: 3s
This data was developed using Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034, the same antibody clone in a different buffer formulation.
Indirect ELISA antibody dose-response curve using Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034 with antigen at 1000 ng/ml
This data was developed using Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034, the same antibody clone in a different buffer formulation.
Dot blot analysis of pyroglutamate beta amyloid using Anti-Pyroglutamate beta Amyloid antibody [IBR-10-2-3] ab264034 at 1/2000 dilution, followed by a Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated (Goat Anti-Rabbit IgG H&L (HRP) ab97051) at 1/100,000 dilution.
Blocking and diluting buffer and concentration was 5% NFDM/TBST.
Lane 1: beta Amyloid pE3-42 (aa674-713) peptide
Lane 2: beta Amyloid 1-42 (aa672-713) peptide
Exposure time: 3 minutes.
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