beta Amyloid Antibody
beta Amyloid Monoclonal Antibody for IHC, WB, ELISA
Cat no : 60342-1-Ig
A4, AAA, ABETA, ABPP, AD1, AICD 50, AICD 57, AICD 59, AID(50), AID(57), AID(59), Amyloid beta A4 protein, amyloid P, APP, APPI, beta Amyloid, CTFgamma, CVAP, Gamma CTF(50) C31, PN II, PN2, PreA4, Protease nexin II, S APP alpha Soluble APP beta
|Positive WB detected in||Y79 cells, HEK-293 cells|
|Positive IHC detected in||human gliomas tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
60342-1-Ig targets beta Amyloid in WB, IHC, IF, ELISA applications and shows reactivity with human, pig samples.
|Tested Reactivity||human, pig|
|Cited Reactivity||human, mouse|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||beta Amyloid fusion protein Ag0769|
|Full Name||amyloid beta (A4) precursor protein|
|Calculated molecular weight||86.9 kDa|
|Observed molecular weight||100 kDa|
|GenBank accession number||BC004369|
|Gene ID (NCBI)||351|
|Purification Method||Protein A purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Aβ derives from APP via proteolytic cleavage by proteases called α-, β- and γ-secretase. The α-secretase cleavage precludes the formation of Aβ, while the β- and γ-cleavages generate APP components with amyloidogenic features. Amyloid beta A4 precursor protein(APP), encoded by APP gene which locate on human chromosome 21q, is a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. APP expressed in all fetal tissues and is pronounced in brain, kidney, heart and spleen, but weak in liver. Defects in APP are the cause of Alzheimer disease type 1 (AD1).
Sudden unexpected death in early Parkinson's disease: neurogenic or cardiac death?
Aging (Albany NY)
Genomic deletion of TLR2 induces aggravated white matter damage and deteriorated neurobehavioral functions in mouse models of Alzheimer's disease.
CIP2A Causes Tau/APP Phosphorylation, Synaptopathy, and Memory Deficits in Alzheimer's Disease.