Description:

Size: 100ul

Catalog no.: bs-0076R-A594

Price: 380 EUR

Product details

Gene ID Number

351

Modification Site

None

Swiss Prot

P05067

Tested applications

IF(IHC-P)

French translation

anticorps

Modification

Unmodified

Clonality

Polyclonal

Excitation emission

590nm/617nm

Concentration

1ug per 1ul

Conjugated with

ALEXA FLUOR® 594

Target Antigen

beta-Amyloid 1-42

Conjugated

Alexa conjugate 1

Crossreactivity

Human, Mouse, Rat

Recommended dilutions

IF(IHC-P)(1:50-200)

Clone

Polyclonal antibody

Subcellular location

Extracellular, Helical

Purification

Purified by Protein A.

Conjugation

Alexa Fluor,ALEXA FLUOR® 594

Category

Conjugated Primary Antibodies

Host Organism

Rabbit (Oryctolagus cuniculus)

Also known as

Anti-beta-Amyloid 1-42 PAb ALEXA FLUOR 594

Long name

beta-Amyloid 1-42 Antibody, ALEXA FLUOR 594 Conjugated

Specificity

This is a highly specific antibody against beta-Amyloid 1-42.

Cross-reactive species details

Due to limited amount of testing and knowledge, not every possible cross-reactivity is known.

Source

This antibody was obtained by immunization of the host with KLH conjugated synthetic peptide derived from human beta-Amyloid(35-42)

Storage conditions

Store this antibody in aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Keep refrigerated at 2 to 8 degrees Celcius for up to one year.

Properties

For facs or microscopy Alexa 1 conjugate.If you buy Antibodies supplied by Bioss Primary Conjugated Antibodies. ALEXA FLUOR they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

Synonyms

AAA; AD1; PN2; ABPP; APPI; CVAP; ABETA; PN-II; CTFgamma; Amyloid beta A4 protein; APP; Alzheimer disease amyloid protein; Amyloid precursor protein; Beta-amyloid precursor protein; Cerebral vascular amyloid peptide; PreA4; Protease nexin-II; A4

Background of the antigen

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-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. 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. Beta-amyloid 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. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses.