|Tested species reactivity||Human|
|Published species reactivity||Mouse, Human|
|Host / Isotype||Mouse / IgG1, kappa|
|Immunogen||Rec-beta-amyloid precursor protein (beta-APP 695)|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|ELISA (ELISA)||0.1-0.5 ug/ml|
|Immunofluorescence (IF)||Assay Dependent|
|Immunohistochemistry (IHC)||5-10 ug/ml|
|Western Blot (WB)||2 µg/mL|
Amyloid beta peptide is the major constituent of amyloid plaques in the brains of individuals afflicted with Alzheimer"e;s disease. This peptide is generated from the beta-amyloid precursor protein (beta APP) in a two-step process. The first step involves cleavage of the extracellular, amino-terminal domain of beta APP. Protein cleavage is performed by an aspartyl protease termed beta-secretase (BACE). This enzyme is synthesized as a propeptide that must be modified to the mature and active form by the prohormone convertase, furin. Beta APP cleavage by the mature form of BACE results in the cellular secretion of a segment of beta APP and a membrane-bound remnant. This remnant is then processed by another protease termed gamma-secretase. Gamma-secretase cleaves an intra-membrane site in the carboxyl-terminal domain of beta APP, thus generating the amyloid beta peptide. Gamma-secretase is believed to be a multi-subunit complex containing presenilin-1 and 2 as central components. Found associated with the presenilins is the transmembrane glycoprotein nicastrin. Nicastrin has been found to bind to the carboxyl-terminus of betaAPP and helps to modulate the production of the amyloid beta peptide.
At the centre of neuronal, synaptic and axonal pathology in murine prion disease: degeneration of neuroanatomically linked thalamic and brainstem nuclei.
13-0200 was used in immunohistochemistry - paraffin section to investigate the spread of neuronal pathology.
|Reis R,Hennessy E,Murray C,Griffin ÉW,Cunningham C||Neuropathology and applied neurobiology (41:780)||2015|
Involvement of receptor tyrosine kinase Tyro3 in amyloidogenic APP processing and β-amyloid deposition in Alzheimer's disease models.
13-0200 was used in western blot to study the role of receptor tyrosine kinase Tyro3 in APP processing and beta amyloid deposition.
|Zheng Y,Wang Q,Xiao B,Lu Q,Wang Y,Wang X||PloS one (7:null)||2012|
Gas1 interferes with AβPP trafficking by facilitating the accumulation of immature AβPP in endoplasmic reticulum-associated raft subdomains.
13-0200 was used in western blot to study the mechanism by which Gas1 blocks the intracellular trafficking of amyloid precursor protein
|Chapuis J,Vingtdeux V,Capiralla H,Davies P,Marambaud P||Journal of Alzheimer's disease : JAD (28:127)||2012|
Growth arrest-specific 1 binds to and controls the maturation and processing of the amyloid-beta precursor protein.
13-0200 was used in immunocytochemistry and western blot to investigate the role of growth arrest-specific 1 in Alzheimer's disease
|Chapuis J,Vingtdeux V,Campagne F,Davies P,Marambaud P||Human molecular genetics (20:2026)||2011|
|Human||1:250||Fe65 is not involved in the platelet-derived growth factor-induced processing of Alzheimer's amyloid precursor protein, which activates its caspase-directed cleavage.||Zambrano N,Gianni D,Bruni P,Passaro F,Telese F,Russo T||The Journal of biological chemistry (279:16161)||2004|
|Mouse||Not Cited||Early-onset and robust amyloid pathology in a new homozygous mouse model of Alzheimer's disease.||Willuweit A,Velden J,Godemann R,Manook A,Jetzek F,Tintrup H,Kauselmann G,Zevnik B,Henriksen G,Drzezga A,Pohlner J,Schoor M,Kemp JA,von der Kammer H||PloS one (4:null)||2009|
|Mouse||1:100||Disruption of corticocortical connections ameliorates amyloid burden in terminal fields in a transgenic model of Abeta amyloidosis.||Sheng JG,Price DL,Koliatsos VE||The Journal of neuroscience : the official journal of the Society for Neuroscience (22:9794)||2002|
|Human||Not Cited||Markers of axonal injury in post mortem human brain.||Sherriff FE,Bridges LR,Gentleman SM,Sivaloganathan S,Wilson S||Acta neuropathologica (88:433)||1995|
Dual-specificity tyrosine(Y)-phosphorylation regulated kinase 1A-mediated phosphorylation of amyloid precursor protein: evidence for a functional link between Down syndrome and Alzheimer's disease.
13-0200 was used in immunocytochemistry to investigate the regulatory link between beta-amyloid precursor protein and dual-specificity tyrosine(Y)-phosphorylation regulated kinase A in Down syndrome brains.
|Ryoo SR,Cho HJ,Lee HW,Jeong HK,Radnaabazar C,Kim YS,Kim MJ,Son MY,Seo H,Chung SH,Song WJ||Journal of neurochemistry (104:1333)||2008|
AAA; ABETA; AD1; alzheimer disease amyloid protein; amyloid beta (A4) precursor protein; amyloid precursor protein; Amyloidogenic glycoprotein AG; APP; beta-amyloid peptide; beta-amyloid peptide(1-40); beta-amyloid peptide(1-42); beta-amyloid precursor protein; cerebral vascular amyloid peptide; CTFgamma; CVAP; Peptidase nexin-II; PN2; preA4; protease nexin-II; testicular tissue protein Li 2
A4; AAA; ABETA; ABPP; AD1; APP; APPI; CTFgamma; CVAP; PN-II; PN2