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|Tested species reactivity||Human|
|Published species reactivity||Human, Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A 30 amino acid synthetic peptide derived from the full length (1-43 amino acid) beta-Amyloid peptide|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|ELISA (ELISA)||Assay Dependent|
|Immunohistochemistry (IHC)||Assay Dependent|
|Immunoprecipitation (IP)||Assay Dependent|
|Western Blot (WB)||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.
|Immunohistochemistry (IHC)||See 9 publications below|
|Immunohistochemistry (Frozen) (IHC (F))||See 5 publications below|
|ELISA (ELISA)||See 1 publications below|
|Immunohistochemistry - Free Floating (IHC (Free))||See 1 publications below|
|Immunohistochemistry (Paraffin) (IHC (P))||See 1 publications below|
|Western Blot (WB)||See 2 publications below|
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.
Tissue transglutaminase-catalysed cross-linking induces Apolipoprotein E multimers inhibiting Apolipoprotein E's protective effects towards amyloid-beta-induced toxicity.
71-5800 was used in immunohistochemistry to study the role of apolipoprotein E in cerebral amyloid angiopathy.
|de Jager M,Drukarch B,Hofstee M,Brevé J,Jongenelen CA,Bol JG,Wilhelmus MM||Journal of neurochemistry (134:1116)||2015|
Butyrylcholinesterase-knockout reduces brain deposition of fibrillar β-amyloid in an Alzheimer mouse model.
71-5800 was used in immunohistochemistry to investigate butyrylcholinesterase activity in a mouse model of Alzheimer's disease.
|Reid GA,Darvesh S||Neuroscience (298:424)||2015|
Vascular pathology of 20-month-old hypercholesterolemia mice in comparison to triple-transgenic and APPSwDI Alzheimer's disease mouse models.
71-5800 was used in immunohistochemistry to investigate hypercholesterolemia at various stages of Alzheimer's disease
|Hohsfield LA,Daschil N,Orädd G,Strömberg I,Humpel C||Molecular and cellular neurosciences (63:83)||2014|
D-Ala2GIP facilitated synaptic plasticity and reduces plaque load in aged wild type mice and in an Alzheimer's disease mouse model.
71-5800 was used in immunohistochemistry to test if D-Ala2GIP protects mice with advanced staged Alzheimer's disease.
|Faivre E,Hölscher C||Journal of Alzheimer's disease : JAD (35:267)||2013|
Tissue transglutaminase colocalizes with extracellular matrix proteins in cerebral amyloid angiopathy.
71-5800 was used in immunohistochemistry to determine the distribution pattern, cellular source, and activity of tissue transglutaminase in cerebral amyloid angiopathy, Alzheimer's disease, and hereditary cerebral hemorrhage with amyloidosis of the Dutch type cases.
|de Jager M,van der Wildt B,Schul E,Bol JG,van Duinen SG,Drukarch B,Wilhelmus MM||Neurobiology of aging (34:1159)||2013|
Evaluation of the effects of testosterone and luteinizing hormone on regulation of β-amyloid in male 3xTg-AD mice.
71-5800 was used in immunohistochemistry to examine how changes in testosterone and luteinizing hormone contribute to Alzheimer's disease.
|Rosario ER,Carroll JC,Pike CJ||Brain research (1466:137)||2012|
An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers.
71-5800 was used in immunohistochemistry to investigate dysregulated insulin signaling in Alzheimer's disease and diabetes.
|Bomfim TR,Forny-Germano L,Sathler LB,Brito-Moreira J,Houzel JC,Decker H,Silverman MA,Kazi H,Melo HM,McClean PL,Holscher C,Arnold SE,Talbot K,Klein WL,Munoz DP,Ferreira ST,De Felice FG||The Journal of clinical investigation (122:1339)||2012|
Effects of aromatase inhibition versus gonadectomy on hippocampal complex amyloid pathology in triple transgenic mice.
71-5800 was used in immunohistochemistry to assess the effects of depleting both circulating and brain estrogen levels in a mouse model of Alzheimer's disease.
|Overk CR,Lu PY,Wang YT,Choi J,Shaw JW,Thatcher GR,Mufson EJ||Neurobiology of disease (45:479)||2012|
Selective estrogen receptor modulators differentially regulate Alzheimer-like changes in female 3xTg-AD mice.
71-5800 was used in immunohistochemistry to assess the use of selective estrogen receptor modulators using a murine model of Alzheimer's disease.
|Carroll JC,Pike CJ||Endocrinology (149:2607)||2008|
Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - frozen section to study the role of soluble mutant amyloid precursor protein on cognitive function and synaptic structure
|Fowler SW,Chiang AC,Savjani RR,Larson ME,Sherman MA,Schuler DR,Cirrito JR,Lesné SE,Jankowsky JL||The Journal of neuroscience : the official journal of the Society for Neuroscience (34:7871)||2014|
Liraglutide can reverse memory impairment, synaptic loss and reduce plaque load in aged APP/PS1 mice, a model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - frozen section to test if Liraglutide has restorative effects in late-stage Alzheimer's disease in mice.
|McClean PL,Hölscher C||Neuropharmacology (76 Pt A:57)||2014|
A novel retro-inverso peptide inhibitor reduces amyloid deposition, oxidation and inflammation and stimulates neurogenesis in the APPswe/PS1ΔE9 mouse model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - frozen section to study the use of a retro-inverso peptide inhibitor to treat a murine model of Alzheimer's disease.
|Parthsarathy V,McClean PL,Hölscher C,Taylor M,Tinker C,Jones G,Kolosov O,Salvati E,Gregori M,Masserini M,Allsop D||PloS one (8:null)||2013|
Butyrylcholinesterase is associated with β-amyloid plaques in the transgenic APPSWE/PSEN1dE9 mouse model of Alzheimer disease.
71-5800 was used in immunohistochemistry - frozen section to investigate the role of BuChE using the APPSWE/PSENdE9 transgenic mouse model.
|Darvesh S,Cash MK,Reid GA,Martin E,Mitnitski A,Geula C||Journal of neuropathology and experimental neurology (71:2)||2012|
The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - frozen section to examine the effects of peripherally injected liraglutide in an Alzheimer mouse model.
|McClean PL,Parthsarathy V,Faivre E,Hölscher C||The Journal of neuroscience : the official journal of the Society for Neuroscience (31:6587)||2011|
Cholinergic degeneration is associated with increased plaque deposition and cognitive impairment in APPswe/PS1dE9 mice.
71-5800 was used in ELISA to study cholinergic dysfunction in a murine model of Alzheimer's disease.
|Laursen B,Mørk A,Plath N,Kristiansen U,Bastlund JF||Behavioural brain research (240:146)||2013|
The effect of ageing on neurogenesis and oxidative stress in the APP(swe)/PS1(deltaE9) mouse model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - free floating to examine how ageing affects neurogenesis and oxidative stress in a mouse model of Alzheimer's disease.
|Hamilton A,Holscher C||Brain research (1449:83)||2012|
Effects of NK-4 in a transgenic mouse model of Alzheimer's disease.
71-5800 was used in immunohistochemistry - paraffin section to report the effects of NK-4 on the toxicity of Aβ, on cognitive function, and Aβ concentration in a mouse model of Alzheimer's disease.
|Ohta H,Arai S,Akita K,Ohta T,Fukuda S||PloS one (7:null)||2012|
22R-Hydroxycholesterol protects neuronal cells from beta-amyloid-induced cytotoxicity by binding to beta-amyloid peptide.
71-5800 was used in western blot to elucidate the mechanism of action of 22R-hydroxycholesterol on Abeta-mediated toxicity.
|Yao ZX,Brown RC,Teper G,Greeson J,Papadopoulos V||Journal of neurochemistry (83:1110)||2002|
Rapid detection of protein aggregates in the brains of Alzheimer patients and transgenic mouse models of amyloidosis.
71-5800 was used in western blot to develop a novel method for the rapid detection of beta-amyloid aggregates in Alzheimer's patients and transgenic mouse models.
|Xu G,Gonzales V,Borchelt DR||Alzheimer disease and associated disorders (16:191)||2002|
AAA; ABETA; ABPP; AD1; Alzheimer disease amyloid protein; amyloid beta (A4) precursor protein; Amyloid beta A4 protein; amyloid precursor protein; Amyloidogenic glycoprotein AG; APP; APPI; 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; PN-II; PN2; PreA4; Protease nexin-II; testicular tissue protein Li 2
A4; AAA; ABETA; ABPP; AD1; APP; APPI; CTFgamma; CVAP; PN-II; PN2