Anti-beta Amyloid antibody [DE2B4],Abcam,AB11132

What is this antibody validated in? Anti-beta Amyloid antibody [DE2B4] (ab11132) is a mouse monoclonal antibody and is validated for use in Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC-P), Immunohistochemistry (IHC-Fr), Immunocytochemistry/immunofluorescence (ICC/IF) in Human samples. What is the molecular weight of beta Amyloid? Anti-beta Amyloid [DE2B4] (ab11132) specifically detects a band for beta Amyloid (UniProt: P05067) at a molecular weight of 87kDa. Trusted by the scientific community Anti-beta Amyloid [DE2B4] (ab11132) was first used in a scientific publication in 2004 and has been cited over 30 times in peer-reviewed journals. Reviewed by scientists Anti-beta Amyloid [DE2B4] (ab11132) has over 5 independent reviews from customers. Other related products We have a range of other formats of antibody clone [DE2B4] also available for your convenience: ab11132, HRP - ab187908

Host

Mouse

Reactivity

Human

Application

IP, ICC/IF, WB, IHC-P, IHC-Fr

Platform ID

BAB224336618

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-beta Amyloid antibody [DE2B4]
Cat. No.AB11132
HostMouse
IsotypeIgG1
ReactivityHuman
ApplicationIP, ICC/IF, WB, IHC-P, IHC-Fr
ClonalityMonoclonal
Clone NumberDE2B4
Concentration1 mg/mL Batch dependent concentration
ImmunogenSynthetic Peptide within Human APP aa 1-50. The exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationPreservative: 0.09% Sodium azide Constituents: PBS
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data 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. See full target information APP

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