Validation Data Gallery
|Positive WB detected in||Y79 cells, pig brain tissue, HEK-293 cells, rabbit brain tissue, rat brain tissue|
|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 APP in WB, IP, IHC, IF, ELISA applications and shows reactivity with human, pig, rat, rabbit samples.
|Tested Reactivity||human, pig, rat, rabbit|
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||APP fusion protein Ag0769|
|Full Name||amyloid beta (A4) precursor protein|
|Calculated molecular weight||87 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. 20ul sizes contain 0.1% BSA.|
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).
Gamma frequency light flicker regulates amyloid precursor protein trafficking for reducing β-amyloid load in Alzheimer's disease model.
Metformin activates chaperone-mediated autophagy and improves disease pathologies in an Alzheimer disease mouse model.
CIP2A Causes Tau/APP Phosphorylation, Synaptopathy, and Memory Deficits in Alzheimer's Disease.
Aging (Albany NY)
Genomic deletion of TLR2 induces aggravated white matter damage and deteriorated neurobehavioral functions in mouse models of Alzheimer's disease.
Front Aging Neurosci
Agomelatine Prevents Amyloid Plaque Deposition, Tau Phosphorylation, and Neuroinflammation in APP/PS1 Mice.
Sarsasapogenin attenuates Alzheimer-like encephalopathy in diabetes.
The reviews below have been submitted by verified Proteintech customers who received an incentive forproviding their feedback.
Jinwei (Verified Customer) (10-01-2021)
The Beta Amyloid Monoclonal antibody works fine.