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|Tested species reactivity||Human|
|Published species reactivity||Mouse , Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||The antiserum was produced against a chemically synthesized peptide corresponding to amino acids 1-40 of human beta-Amyloid (A-beta).|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.3|
|Tested Applications||Dilution *|
|Dot blot (DB)||Assay Dependent|
|Immunohistochemistry (IHC)||Assay Dependent|
|Radioimmune Assays (RIA)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
No significant cross-reactivity to beta-Amyloid 42 has been observed. Previous lots of this antibody recognized the sequence of beta-Amyloid [1-40] in the region from amino acids 15-30. No blocking activity was observed with beta-Amyloid [1-12] whereas the peptides beta-Amyloid [14-35], beta-Amyloid [15-28], beta-Amyloid [17-30] and Beta-Amyloid [1-40] were all able to block antibody activity.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Histamine induces Egr-1 expression in human aortic endothelial cells via the H1 receptor-mediated protein kinase Cdelta-dependent ERK activation pathway.
||Hao F,Tan M,Xu X,Cui MZ||The Journal of biological chemistry (283:26928)||2008|
Apolipoprotein E4 influences amyloid deposition but not cell loss after traumatic brain injury in a mouse model of Alzheimer's disease.
||Hartman RE,Laurer H,Longhi L,Bales KR,Paul SM,McIntosh TK,Holtzman DM||The Journal of neuroscience : the official journal of the Society for Neuroscience (22:10083)||2002|
Human and murine ApoE markedly alters A beta metabolism before and after plaque formation in a mouse model of Alzheimer's disease.
||Fagan AM,Watson M,Parsadanian M,Bales KR,Paul SM,Holtzman DM||Neurobiology of disease (9:305)||2002|
Passive immunization against beta-amyloid peptide protects central nervous system (CNS) neurons from increased vulnerability associated with an Alzheimer's disease-causing mutation.
||Mohajeri MH,Saini K,Schultz JG,Wollmer MA,Hock C,Nitsch RM||The Journal of biological chemistry (277:33012)||2002|
CTFgamma, ABPP, PN2, PN-II, AAA, CVAP, APPI, ABETA, AD1
alzheimer disease amyloid protein, amyloid beta A4 protein, beta-amyloid peptide, cerebral vascular amyloid peptide, peptidase nexin-II, preA4, protease nexin-II, AAA, ABETA, AD1, CTFgamma, CVAP, PN2, APP, Amyloidogenic glycoprotein AG, Amyloid beta A4 protein, amyloid beta (A4) precursor protein, Peptidase nexin-II